Exanthema

Cardiac arrest Drug related eosinophilia with systemic symptoms (DRESS) Symmetrical drug-related intertriginous and flexural exanthema (SDRIFE) Vasculitis... 

Atypical manifestations reported Maculopapular exanthema and time course resembles drug allergy... 

The most common clinical picture of non-immediate RCM reactions is a macu-lopapular exanthema, which resembles other drug-induced T-cell-mediated hypersensitivity reactions. The reported onset of skin eruptions 2-10 days after the first exposure to a RCM and 1-2 days after re-exposure to the same substance is typical for an allergic drug reaction with a sensitization phase. 

Previous reactors are at high risk for a new reaction. In many cases reported, re-administration of the culprit contrast medium to patients with a previous non-immediate exanthema resulted in a repeat reaction [1]. In some (but not all) cases, a more severe reaction with subsequent RCM exposure has been described. After provocation tests, a re-appearance of the exanthemas after intravenous administration of the culprit contrast medium has been reported in patients with previous contrast medium-induced eruptions [1]. 

Hematology and clinical chemistry should be considered in more severe exanthema, as systemic involvement has been described [1]. A skin biopsy may sometimes be needed for differential diagnosis. 

Christiansen C, Dreborg S. Pichler WJ. Ekeli H Macular exanthema appearing 5 days after X-ray contrast medium administration. Eur Radiol 2002 12(suppl 3) S94-S97. 

Arnold AW, Hausermann P, Bach S, Bircher AJ Recurrent flexural exanthema (SDRIFE or baboon syndrome) after administration of two different iodinated radiocontrast media. Dermatology 2007 214 89-93. Laroche D Immediate reactions to contrast media mediator release and value of diagnostic testing. Toxicology 2005 209 193-194. 

NSAIDs can induce a number of other adverse reactions, including bleeding disorders, anemia, thrombocytopenia, erythema nodosum, erythema multiforme, fixed drug eruptions, toxic epidermal necrolysis, Stevens-Johnson syndrome, leukocytocla-sitc vasculitis, recurrent fever with exanthema and, of course, the well-known gastric cytotoxicity. 

Suggested Alternatives for Differential Diagnosis Rinderpest, infectious bovine rhino-tracheitis, bovine herpes mammillitis, malignant catarrhal fever, Peste des petits ruminants, vesicular stomatitis, bluetongue, bovine viral diarrhea, and foot rot in cattle, vesicular exanthema of swine, swine vesicular disease, and foreign bodies or trauma. 

Type 3, immune complex vasculitis (serum sickness, Arthus reaction). Drug-antibody complexes precipitate on vascular walls, complement is activated, and an inflammatory reaction is triggered. Attracted neutrophils, in a futile attempt to phagocytose the complexes, liberate lysosomal enzymes that damage the vascular walls (inflammation, vasculitis). Symptoms may include fever, exanthema swelling of lymph nodes, arthritis, nephritis, and neuropathy. 

Undesired effects. The magnitude of the antihypertensive effect of ACE inhibitors depends on the functional state of the RAA system. When the latter has been activated by loss of electrolytes and water (resulting from treatment with diuretic drugs), cardiac failure, or renal arterial stenosis, administration of ACE inhibitors may initially cause an excessive fall in blood pressure. In renal arterial stenosis, the RAA system may be needed for maintaining renal function and ACE inhibitors may precipitate renal failure. Dry cough is a fairly frequent side effect, possibly caused by reduced inactivation of kinins in the bronchial mucosa. Rarely, disturbances of taste sensation, exanthema, neutropenia, proteinuria, and angioneurotic edema may occur. In most cases, ACE inhibitors are well tolerated and effective. Newer analogues include lisinopril, perindo-pril, ramipril, quinapril, fosinopril, benazepril, cilazapril, and trandolapril. 

Speciai risk Use with caution in the following situations Nonspecific ulcerative colitis if there is a probability of impending perforation, abscess, or other pyogenic infection diverticulitis fresh intestinal anastomoses hypertension CHF thromboembolitic tendencies thrombophlebitis osteoporosis exanthema Cushing syndrome antibiotic-resistant infections convulsive disorders metastatic carcinoma myasthenia gravis vaccinia varicella diabetes mellitus hypothyroidism, cirrhosis (enhanced effect of corticosteroids). 

Adverse effects include breast discomfort, pruritus, exanthema, thrombophlebitis and local skin irritation, increased risk of gall stones. 

A 43-year-old man developed generalized exanthema pustulosis 48 hours after the start of acarbose therapy (66). The lesions disappeared within 1 week after stopping acarbose. He was not retested. 

Fixed eruptions (drug exanthemas) with mostly few demarcated, painful lesions, usually located in intertriginous skin regions (genital area, mucous membranes). With repeated exposure, these typically recur at the same sites. 

Lindner K, Prater E, Schubert H, Siegmund S. Arzneimittel exanthem auf chlorhydrat. [Drug exanthema due to chloral hydrate.] Dermatol Monatsschr 1990 176(8) 483-5. 

Fever and toxemia, 7-8 days postexposure, with eruption of viral exanthema 7-17 days of incubation, abrupt fever, malaise, headache, prostration, backache, with eruption of amaculopapular rash on the mouth and oropharynx, face, forearms, trunk, and lower extremities (Rajagopalan, 2002). 

Exanthemas are observed as prodromal skin symptoms in acute viral hepatitis (5-20% of cases). They can be manifested as urticaria, scarlatinoid or morbilliform exanthemas as well as varicella and erythematous multiform rashes. 

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