Penicillin skin eruptions with

Many drug reactions cause pruritus, mainly in connection with skin eruptions, e.g. urticaria in penicillin-V allergy. Morphine is an example of a drug which may produce pmritus without other skin involvement. 

The incidence of nonallergic ampicillin eruptions is 40 to 100% in patients with concomitant Epstein-Barr virus (mononucleosis), cytomegalovirus, acute lymphocytic leukemia, lymphoma, or reticulosarcoma. Nonallergic penicillin-associated rashes are characteristically morbilliform (symmetrical, erythematous, confluent, maculopapular) eruptions on the extremities. The onset of typical nonallergic eruptions is more than 72 hours after (3-lactam exposure. The mechanism for the nonurticarial ampicillin rash is not known and is not related to IgE or type I hypersensitivity. Penicillin skin tests are not useful in the evaluation of nonurticarial ampicillin rashes. Patients with a history of nonurticarial ampicillin rashes may receive other (3-lactam antibiotics without greater risk of subsequent serious allergic reactions. 

The newer derivatives seem less likely to cause hypersensitivity reactions, perhaps because the protein adducts generated are shorter lived. All four types of hypersensitivity reaction have been observed with penicillin. Thus, high doses may cause hemolytic anemia and immune complex disease and cell-mediated immunity may give rise to skin rashes and eruptions, and the most common reactions are urticaria, skin eruptions, and arthralgia. Antipenicillin IgE antibodies have been detected consistently with an anaphylactic reaction. The anaphylactic reactions (type 1 see above), which occur in 0.004% to 0.015% of patients, may be life threatening. 

An interesting phenomenon is the fact that patients treated with penicillin while infected with Epstein Barr virus are more likely to develop mobilliform eruption, but at the same time lack penicUlin-specific IgE antibodies. further, these patients appear to tolerate future course of penicillin therapy quite well. The actual mechanism of this infection-associated phenomenon is unknown but viral infection is associated with increased release of interferons. Interferons have been reported to increase MHC expression on the surface membranes of APC in the skin and thus increase activity of dermal immune activity. 

The most serious hypersensitivity reactions produced by the penicillins are angioedema and anaphylaxis. Acute anaphylactic or anaphylactoid reactions to the penicillins constitute the most important immediate danger connected with their use. Among all drugs, the penicillins are most often responsible for this type of untoward effect. Anaphylactoid reactions to penicillins may occur at any age their incidence is thought to be 0.004-0.04%. About 0.001% of patients treated with these agents die from anaphylaxis. Anaphylaxis most often has followed parenteral use but also has been observed after oral or intradermal administration. The most dramatic reaction is sudden hypotension and death. In other instances, bronchoconstriction with severe asthma abdominal pain, nausea, and vomiting extreme weakness or diarrhea and purpuric skin eruptions have characterized the anaphylactic episodes. 

Penicillins can cause all four types of hypersensitivity responses provoking type I IgE-mediated reactions such as urticaria, angioedema, asthma, and anaphylaxis type n antibody-mediated hemolytic anemia and thrombocytopenia type III immune complex-mediated serum sickness-like reactions and vasculitis and type IV T cell-mediated contact dermatitis, rashes, and other skin eruptions (refer to Chaps. 2 and 3). Table 5.1 lists clinical adverse reactions, together with their immune... 

Mechanisms of non-immediate reactions are unclear but may be immunological and non-immunological. Delayed reactions of the IgE type are known (131). Aminopenicillins seem to be an important cause of non-immediate reactions (132-134). The morbilliform rash that begins 1-10 days after amoxicillin can be caused by a delayed cell-mediated immune reaction (135) as can fixed drug eruptions (136,137), toxic epidermal necrolysis (138-140), bullous erythroderma (141), and contact eczema (142). Investigation of these disorders should include delayed readings of skin tests (135). In patients with chronic urticaria, penicillin allergy was demonstrated by cutaneous tests. 

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