Serum-sickness syndrome

Rashes, angioedema, serum sickness syndrome, anaphylaxis or asthma characteristics of classic protein allergy... 

The serum-sickness syndrome (type III). This occurs about 1-3 weeks after administration. Treatment is by an adrenal steroid, and as above if there is urticaria. 

Allergic reactions (e.g., skin rash) are relatively common. In addition, serum sickness syndrome, jaundice, hypoprothrombinemia. thrombocytopenia, polyarteritis, and lupus erythematosus can occur. 

Sulphonamides are usually the cause of type III or type IV allergic reactions, such as serum-sickness syndrome, or probably, the majority of maculopapular rashes. 

The most frequent adverse effects are local reactions at the injection site (pain, tenderness, erythema, swelling, and pruritus), fevers (greater than 37.5°C or 99.5°F), headaches, dizziness, and irritability. Anaphylaxis and hypersensitivity reactions have been reported rarely and occur within a few hours after vaccine administration. In rare instances, a serum sickness-like apparent hypersensitivity syndrome (arthralgia, urticaria, ecchymoses, erythema multiforme, and erythema nodosum) has been... 

These reactions involve a serum sickness like syndrome (e.g., arthralgias, fever, malaise, and urticaria) that usually develops 7 to 14 days after exposure to the causative antigen. 

Rash and accompanying events Seven percent of patients taking fluoxetine have developed a rash or urticaria. Several other patients have had systemic syndromes suggestive of serum sickness. 

Misceiianeous Brown-black microscopic discoloration of thyroid glands (prolonged therapy), decreased hearing, fever, lupus-like syndrome, secretion discoloration, serum sickness-like syndrome, tinnitus, tooth discoloration, vulvovaginitis. 

The drugs inducing serum sickness are sulfonamides, penicillin etc. Sulfonamides also cause Stevens-Johnson syndrome, a form of immune vasculitis, which is characterized by the reactions including arthritis, nephritis, myocarditis and certain mental symptoms. 

The common side effects are nausea and vomiting. The others are allergic symptoms including drug fever, skin rash, urticaria, eosinophilia, photosensitization reactions, serum sickness like syndrome. Stevens-Johnson syndrome and exfoliative dermatitis are also common with longer acting agents. 

Adverse reactions to cefuroxime have been generally mild and transient in nature. As with other cephalosporins there have been rare reports of erythema multiforme, Steven-Johnson syndrome, toxic epidermal necrolysis (exanthematic necrolysis) and hypersensitivity reactions including skin rashes, urticaria, pruritus, drug fever, serum sickness and very rarely anaphylaxis. 

Immune vasculitis can also be induced by drugs. The sulfonamides, penicillin, thiouracil, anticonvulsants, and iodides have all been implicated in the initiation of hypersensitivity angiitis. Erythema multiforme is a relatively mild vasculitic skin disorder that may be secondary to drug hypersensitivity. Stevens-Johnson syndrome is probably a more severe form of this hypersensitivity reaction and consists of erythema multiforme, arthritis, nephritis, central nervous system abnormalities, and myocarditis. It has frequently been associated with sulfonamide therapy. Administration of nonhuman monoclonal or polyclonal antibodies such as rattlesnake antivenin may cause serum sickness. 

A delayed serum sickness-like reaction may occur 1-2 weeks after anti-TNF therapy in 1% of patients. These reactions consist of myalgia, arthralgia, jaw tightness, fever, rash, urticaria, and edema and usually require discontinuation of that agent. Positive antinuclear antibodies and anti-double-stranded DNA develop in a small number of patients. Development of a lupus-like syndrome is rare and resolves after discontinuation of the drug. 

The major adverse reactions to the penicillins are hypersensitivity responses. Manifestations of hypersensitivity inclnde nrticaria, angioedema, and anaphylaxis (type 1 reaction) hemolytic anemia (type 11 reaction) interstitial nephritis, vascnlitis, and serum sickness (type 111 reaction) and contact dermatitis or Stevens-Johnson syndrome (type IV reaction). A maculopapular rash occnrs late in the treatment course of 2% to 3% of patients receiving a penicillin drug. Once a patient has had a hypersensitivity response to a penicillin, it is probable, bnt not certain, that a reaction will occur with exposure to the same penicillin or to any other penicillin. Intradermal skin tests can predict whether a patient is at risk for developing a hypersensitivity reaction to the penicillins. If the resnlts are positive, penicillins should generally be avoided. 

Parra FM, Igea JM, Martin JA, Alonso MD, Lezaun A, Sainz T. Serum sickness-Uke syndrome associated with cefaclor therapy. AUergy 1992 47(4 Pt 2) 439-40. 

Dermatological adverse effects are not uncommon with griseofulvin and are of considerable variety. The following have been described urticaria (28,29), photosensitivity eruptions (30), erythema multiforme (31), morbilliform rashes (32), serum sickness-like reactions (33), fixed drug eruption (29,34,35), Stevens-Johnson syndrome (36), vasculitis (37), toxic epidermal necrolysis (38,39), and lupus erythematosus (40,41). 

Immunoallergic reactions have been reported with minocycline and include lupus-like syndrome, autoimmune hepatitis, eosinophilic pneumonia, hypersensitivity syndrome, a serum sickness-like illness (29), and Sweet s syndrome (SEDA-21, 262) (SEDA-22, 271). Over 60 minocycline-induced cases of lupus-like syndrome and 24 cases of minocycline-induced autoimmune hepatitis were found in a review of the literature (30). In 13 patients, both disorders co-existed. These patients had symmetrical polyarthralgia/polyarthritis, raised liver enzymes, and positive antinuclear antibodies they were also generally antihistone-negative, and only two patients had p-ANCA antibodies. Minocycline-related lupus can also occur in adolescents (31). 

The authors reviewed some other cases of serum sickness after the use of minocycline. They suggested that the syndrome is under-reported, either because of unawareness that it can be an adverse effect or lack of willingness of physicians to document the event. 

Cuevas M, Fraj J. Serum sickness-like syndrome associated with minocycline therapy. Allergy 1990 45(4) 313-15. 

Antimuromonab IgE antibodies have been identified after 10-25 days of treatment in six of 181 patients, and only in those with high titers of antimuromonab IgG antibodies (34). Immediate IgE-mediated anaphylactic reactions, namely anaphylactic shock, bronchospasm, urticaria, have been rarely reported and have sometimes been difficult to differentiate from the cytokine-release syndrome (35,36). Late-onset reactions after the first week of treatment, including cutaneous erythema, a fall in blood pressure, or serum sickness-hke reactions, are infrequent (37). 

Desensitization is not effective in non-IgE-mediated reactions and should therefore not be attempted, for example in cases of serum sickness-like sjmdromes or Stevens-Johnson syndrome. 

Brandslund I, Petersen PH, Strange P, Hole P, Worth V. Haemolytic uraemic syndrome and accumulation of haemoglobin-haptoglobin complexes in plasma in serum sickness caused by penicillin drugs. Haemostasis 1980 9(4) 193-203. 

The phenytoin hypersensitivity syndrome ranges from a simple rash to a fulminant fatal illness with exfoliative dermatitis, vasculitis, and disseminated intravascular coagulation. Features include variable combinations of fever, eosinophilia, lymphadenopathy, hepatosplenome-galy, atypical lymphocytes, blood dyscrasias, serum sickness, hepatitis, and renal insufficiency. 

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