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Hub AI
Serum sickness AI simulator
(@Serum sickness_simulator)
Hub AI
Serum sickness AI simulator
(@Serum sickness_simulator)
Serum sickness
Serum sickness in humans is a reaction to proteins in antiserum derived from a non-human animal source, occurring an average of 8 days after exposure. Symptoms often include a rash, joint pain, fever, and lymphadenopathy. It is a type of hypersensitivity, specifically immune complex hypersensitivity (type III). The term serum sickness–like reaction (SSLR) is occasionally used to refer to similar illnesses that arise from the introduction of certain non-protein substances, such as penicillin.
Serum sickness may be diagnosed based on the symptoms, and using a blood test and a urine test. It may be prevented by not using an antitoxin derived from animal serum, and through prophylactic antihistamines or corticosteroids. It usually resolves naturally, but may be treated with corticosteroids, antihistamines, analgesics, and (in severe cases) prednisone. It was first characterized in 1906.
Signs and symptoms can take as long as 14 days after exposure to appear. They may include signs and symptoms commonly associated with hypersensitivity or infections. Common symptoms include:
Other symptoms include glomerulonephritis, blood in the urine, splenomegaly (enlarged spleen), hypotension (decreased blood pressure), and in serious cases circulatory shock.
Rarely, serum sickness can have severe complications. These include neuritis, myocarditis, laryngeal oedema, pleurisy, and Guillain–Barré syndrome.
Serum sickness is a type III hypersensitivity reaction, caused by immune complexes. When an antiserum is given, the human immune system can mistake the proteins present for harmful antigens. The body produces antibodies, which combine with these proteins to form immune complexes. These complexes precipitate, enter the walls of blood vessels, and activate the complement cascade, initiating an inflammatory response and consuming much of the available complement component 3 (C3). They can be found circulating in the blood, which differentiates serum sickness from serum sickness-like reaction. The result is a leukocytoclastic vasculitis. This results in hypocomplementemia, a low C3 level in serum. They can also cause more reactions, causing the typical symptoms of serum sickness. This is similar to a generalised Arthus reaction.
Serum sickness is usually a result of exposure to antibodies derived from animals. These sera or antitoxins are generally given to prevent or treat an infection or envenomation (venomous bite).
Serum sickness may be caused by some routine medications. Some of the drugs associated with serum sickness are:
Serum sickness
Serum sickness in humans is a reaction to proteins in antiserum derived from a non-human animal source, occurring an average of 8 days after exposure. Symptoms often include a rash, joint pain, fever, and lymphadenopathy. It is a type of hypersensitivity, specifically immune complex hypersensitivity (type III). The term serum sickness–like reaction (SSLR) is occasionally used to refer to similar illnesses that arise from the introduction of certain non-protein substances, such as penicillin.
Serum sickness may be diagnosed based on the symptoms, and using a blood test and a urine test. It may be prevented by not using an antitoxin derived from animal serum, and through prophylactic antihistamines or corticosteroids. It usually resolves naturally, but may be treated with corticosteroids, antihistamines, analgesics, and (in severe cases) prednisone. It was first characterized in 1906.
Signs and symptoms can take as long as 14 days after exposure to appear. They may include signs and symptoms commonly associated with hypersensitivity or infections. Common symptoms include:
Other symptoms include glomerulonephritis, blood in the urine, splenomegaly (enlarged spleen), hypotension (decreased blood pressure), and in serious cases circulatory shock.
Rarely, serum sickness can have severe complications. These include neuritis, myocarditis, laryngeal oedema, pleurisy, and Guillain–Barré syndrome.
Serum sickness is a type III hypersensitivity reaction, caused by immune complexes. When an antiserum is given, the human immune system can mistake the proteins present for harmful antigens. The body produces antibodies, which combine with these proteins to form immune complexes. These complexes precipitate, enter the walls of blood vessels, and activate the complement cascade, initiating an inflammatory response and consuming much of the available complement component 3 (C3). They can be found circulating in the blood, which differentiates serum sickness from serum sickness-like reaction. The result is a leukocytoclastic vasculitis. This results in hypocomplementemia, a low C3 level in serum. They can also cause more reactions, causing the typical symptoms of serum sickness. This is similar to a generalised Arthus reaction.
Serum sickness is usually a result of exposure to antibodies derived from animals. These sera or antitoxins are generally given to prevent or treat an infection or envenomation (venomous bite).
Serum sickness may be caused by some routine medications. Some of the drugs associated with serum sickness are: