Valdecoxib-associated acute generalized exanthematous pustulosis

Byerly, Faera L.; Nelson, Kelly C.; Granko, Robert P.; Morrell, Dean S.; Cairns, Bruce A.

doi:10.1016/j.burns.2004.10.017

Cited by 32 publications

(37 citation statements)

References 24 publications

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“…5 Dysfunction of multiple organ systems is rare, and only a few cases in the literature report hemodynamic disturbances. [6][7][8] We believe that the abnormalities observed on the initial chest scans for our patient were related to cardiogenic pulmonary edema with systemic inflammatory response syndrome-associated increased vascular permeability. The severity and prolonged duration of the inflammatory response in our patient probably led to cardiac dysfunction.…”

Section: Clinical Findingsmentioning

confidence: 77%

Acute generalized exanthematous pustulosis with severe organ dysfunction

Leclair¹,

Maynard²,

St-Pierre³

2009

Canadian Medical Association Journal

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A 53-year-old man was transferred to our intensive care unit for a generalized exanthem with systemic inflammatory response syndrome. His medical history included a possible disseminated infection of herpes zoster 15 years before the current admission. He had no history of psoriasis, cutaneous drug reaction, immune suppression or heart disease. Before the current incident, he had not been using any prescribed or over-the-counter medications.Seven days before admission, the patient was bitten on his finger by a spider. He reported pain at the site, and there was a necrotic crust. His primary care physician prescribed cefprozil. A few hours after the first dose, a rash developed. The rash was described as a generalized exanthem with nonfollicular superficial pustules and fever. Based on a working diagnosis of recurrent herpes zoster, he was given famciclovir.Two days before admission to our intensive care unit, the patient was admitted to another centre with high fever, fatigue and persistent skin lesions. Because of fever, leukocytosis and pustules, an infectious cause was suspected. Antibiotic coverage was broadened to include piperacillin-tazobactam and moxifloxacin. The results of tests for infectious and immunosupressive diseases were negative. A computerized tomography (CT) scan of the patient's chest showed alveolar opacities with a ground-glass appearance in both upper lungs. A CT scan of the patient's abdomen showed small nonspecific opacities in his liver. The patient was then transferred to our centre.When the patient arrived at our centre, he had a fever (39.9°C) and was tachycardic (130 beats/min) and hypotensive (90/80 mm Hg). His oxygen saturation was 90% on room air. There was no jugular venous distension. The results of a cardiac examination were unremarkable, except for tachycardia. More than 80% of his skin, including his face and scalp, was affected by a generalized erythema with multiple small nonfollicular pustules. An examination of his mucous membranes showed redness of his tongue. He did not have the Nicolsky sign. (The Nikolsky sign is detected by applying pressure to the skin, which causes intraepidermal cleavage that allows the superficial skin to slip free from the deeper layer. It is mainly seen with bullous diseases and toxic epidermal necrolysis.)Important laboratory results are shown in Table 1. An electrocardiogram showed only sinus tachycardia. We suspected a cutaneous drug reaction. The main diagnoses considered at that time were Stevens-Johnson syndrome or toxic epidermal necrolysis and acute generalized exanthematous pustulosis associated with severe systemic inflammatory response syndrome. The results of the CT scan of the patient's chest were suggestive of an acute lung injury. An infectious cause was not likely because all of the cultures were negative. Antibiotics were discontinued, and fluid resuscitation was initiated. A few hours after admission, our patient developed pulmonary edema with acute respiratory failure. Noninvasive positive pressure ventilation and diuretic ...

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Section: Clinical Findingsmentioning

confidence: 77%

Acute generalized exanthematous pustulosis with severe organ dysfunction

Leclair¹,

Maynard²,

St-Pierre³

2009

Canadian Medical Association Journal

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“…The pathomechanisms include a role for T cells, with drug-specific T cells expressing the potent neutrophil-attracting chemokine interleukin 8 115. While CD8 T cells promote local tissue destruction, CD4 T cells recruit neutrophils to the site 117. The histopathological features include spongiform subcorneal and/or intra-epidermal pustules, papillary dermis oedema, perivascular neutrophils and eosinophils and leucocytoclastic vasculitis (fig 3B).…”

Section: Predominantly Pustular Drug Reactionsmentioning

confidence: 99%

Drug-induced cutaneous pathology

Ramdial¹,

Naidoo²

2009

J Clin Pathol

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Drug-induced cutaneous rashes, whether confined to the skin or part of a systemic disease, are characterised by a spectrum of inflammatory disease patterns that include perivascular dermatitis, nodular and diffuse dermatitis, vesiculobullous lesions, pustular eruptions, sclerodermoid reactions, vasculitis, folliculitis/perifolliculitis and panniculitis. While a single drug can elicit a range of reaction patterns, no reaction pattern is specific for a particular drug. Although the temporal link between initiation of drug therapy and the onset of the drug rash is critical to the diagnosis, drug reactions may also occur during the course of chronic drug ingestion. Clues to the drug-induced nature of the cutaneous eruption include the presence of overlapping histological reaction patterns and incongruent clinical and histopathological features. While eosinophils are an important tell-tale sign of a drug-induced reaction, they may also be conspicuous in skin rashes devoid of a drug association. Furthermore, eosinophils may be sparse or absent in some drug exanthems. Heightened awareness of the mimicry of a wide spectrum of cutaneous pathology by an ever-increasing range of therapeutic agents is pivotal to the diagnosis of drug-induced skin pathology.

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“…Valdecoxib induced severe allergic skin reactions [321,322] which, together with an increased risk of cardiovascular side effects [323] was the reason why the compound, together with its prodrug derivative parecoxib, was withdrawn from the market in 2004.…”

Section: Rofecoxibmentioning

confidence: 99%

Analgesics and Antipyretics, 2. Nonsteroidal Anti‐inflammatory Drugs

Friderichs

Christoph

Buschmann

2011

Ullmann's Encyclopedia of Industrial Chemistry

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The article contains sections titled: 1. Introduction 2. Salicylates 3. Para‐Aminophenol Derivatives 4. Anthranilates 5. Arylacetic Acids 6. Arylpropionic Acids 7. Pyrazolinone Derivatives 8. Acidic Enolic Compounds 8.1. Pyrazolidine‐3,5‐diones 8.2. Arylsulfonamides (Oxicames) 9. Other Structures 10. COX‐2 Inhibitors 10.1. Nonselective COXC‐2 Inhibitors 10.2. Selective COX‐2 Inhibitors (Coxibs)

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Valdecoxib-associated acute generalized exanthematous pustulosis

Cited by 32 publications

References 24 publications

Acute generalized exanthematous pustulosis with severe organ dysfunction

Acute generalized exanthematous pustulosis with severe organ dysfunction

Drug-induced cutaneous pathology

Analgesics and Antipyretics, 2. Nonsteroidal Anti‐inflammatory Drugs

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