Cases reported "Drug Eruptions"

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1/11. Pseudoporphyria induced by propionic acid derivatives.

    BACKGROUND: Pseudoporphyria is a photosensitive bullous skin disease that is distinguished from porphyria cutanea tarda (PCT) by its normal porphyrin profile. Drugs are a major cause of this disease, and the list of culprits is continually expanding. Nonsteroidal antiinflammatory agents (NSAIDs), especially naproxen and other propionic acid derivatives, appear to be the most common offenders. OBJECTIVE: The study was carried out to increase awareness about the etiology and characteristic features of pseudoporphyria. methods: We report two cases of pseudoporphyria caused by naproxen and oxaprozin. We review the current English language literature on this entity and discuss its clinical features, histology, ultrastructure, etiology, and pathophysiology. RESULTS: A 44-year-old man taking naproxen for chronic low back pain and a 20-year-old woman on oxaprozin for rheumatoid arthritis presented with tense bullae and cutaneous fragility on the face and the back of the hands. In both, skin biopsy showed a cell-poor subepidermal vesicle with festooning of the dermal papillae. Direct immunofluorescence revealed staining at the dermal-epidermal junction and around blood vessels with IgG in the first case and with IgG, IgA, and fibrin in the second case. urine collections and serum samples yielded normal levels of uro- and coproporphyrins. CONCLUSIONS: Most cases of pseudoporphyria are drug-induced. naproxen, the most common offender, has been associated with a dimorphic clinical pattern: a PCT-like presentation and one simulating erythropoietic protoporphyria in the pediatric population. Other NSAIDs of the propionic acid family can also cause pseudoporphyria.
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2/11. Necrotizing vasculitis of the skin and uterine cervix associated with minocycline therapy for acne vulgaris.

    In recent years, minocycline has become a commonly used agent for the treatment of acne vulgaris and rosacea. With this increased use have come reports of severe and in some cases life-threatening toxicity, often occurring in otherwise healthy young women after prolonged courses of minocycline. These adverse reactions include hepatotoxicity, drug-induced lupus erythematosus, eosinophilic pneumonitis, and hypersensitivity syndrome. We describe a 35-year-old woman who had necrotizing vasculitis of the skin and uterine cervix after 2 years of minocycline therapy for acne vulgaris. skin and cervical biopsies revealed acute inflammation involving through-and-through necrosis of vessel walls with thrombosis, focal fibrinoid change, and a perivascular lymphohistiocytic infiltrate. The disease fully resolved within 3 months of discontinuance of the minocycline therapy. patients should be informed of these rare but potentially serious adverse effects before the initiation of minocycline therapy. Early recognition of these complications can result in complete resolution.
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3/11. Neonatal urticaria due to prostaglandin E1.

    Prostaglandin E1 is commonly used in the management of cyanotic congenital heart disease. While cutaneous flushing and peripheral edema are well recognized side effects of prostaglandin E1 therapy, other cutaneous effects have not been described in the dermatologic literature. We report a neonate with transposition of the great vessels who developed urticaria during treatment with prostaglandin E1.
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4/11. Noninflammatory bullae associated with epsilon-aminocaproic acid infusion.

    Three patients who had cardiac surgery developed a transient, noninflammatory subepidermal bullous eruption on the legs after epsilon-aminocaproic acid infusion. fibrin thrombi were demonstrated in papillary dermal vessels. The use of epsilon-aminocaproic acid as an antifibrinolytic agent may predispose patients to cutaneous vascular thromboses.
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5/11. Psoriasiform eruption induced by propranolol.

    The appearance of a psoriasiform eruption in a seventy-eight year old patient after one year of treatment with propranolol is presented herein. The histologic picture was not compatible with psoriasis vulgaris, although it contained some of the same features. Immunologic investigation revealed immune deposits at the junction of the dermis and epidermis and in blood vessel walls as well as monoclonal gammopathy. The rash, which was followed by a reduction in tear secretion, is suggested to have been a drug reaction associated with propranolol. This is supported by the positive results of a migration inhibiting factor test towards propranolol, the clearing of the eruption which took place three weeks after withdrawal of the drug, and the negative result of the same test obtained soon afterwards.
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6/11. purpura after application of EMLA cream in two children.

    The eutectic mixture of local anesthetic cream, a 1 : 1 mixture of prilocaine and lidocaine, 2.5% each, is frequently used in pediatric and dermatologic practice to obtain local anesthesia. Side effects include transient skin blanching, erythema, urticaria, allergic contact dermatitis, irritant contact dermatitis, hyperpigmentation, and purpura. We report two children with a purpuric reaction after application of this mixture cream. purpura after application of this anesthetic cream is a rare nonallergic reaction and only 17 occurrences have been reported, to our knowledge, in the literature. patch tests could not be performed in our two patients because of lack of parental consent but we suggest that the purpuric reactions were most probably of toxic origin. The pathogenesis of purpura after application of eutectic mixture of local anesthetics cream, which resolves within 2 weeks without dermatologic sequelae and without any specific therapy, is complex. The lesions are probably caused by the direct effect of the cream components on the vessels but many other factors, such as atopic dermatitis, prematurity, subjective predisposition to purpura, trauma, and thrombocytopenia may play important pathogenetic roles.
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7/11. Deposition of immunoglobulin and complement in mucocutaneous lesions related to treatment with D-penicillamine.

    A 23-year-old man suffering from sero-negative rheumatoid arthritis developed severe penicillamine-induced mouth ulcerations and erythematous macules. Immunohistochemical staining in a biopsy specimen from the affected lingual mucosa showed substantial deposition of IgM and C3 in vessel walls below the necrotic epithelium. In the affected skin, irregular granular staining for IgG and IgM along the epidermal basement membrane zone was noted, and granular deposits of IgM were present in small vessels of dermal papillae. The mouth ulcerations healed promptly after withdrawal of the drug, whereas the macules persisted for some months. The immunohistochemical findings indicated that the drug eruptions were related to a vasculitis induced by deposition of immune complexes.
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8/11. hypersensitivity reaction to doxorubicin.

    A 42-year-old woman with synovial sarcoma developed a skin flare during doxorubicin therapy. With a subsequent dose, erythema, urticaria, and asthma occurred, despite pretreatment with antihistamines. skin flares occur in about three percent of patients receiving doxorubicin. Rarely, generalized urticaria, angioneurotic edema, or anaphylaxis occur. Local reactions may represent molecular extravasation through vessels, or histamine release from mast cells or basophils. Generalized reactions may involve alternative complement-activation pathways. Pretreatment with antihistamines or corticosteroids sometimes is helpful in preventing recurrences.
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9/11. Severe exfoliative dermatitis associated with hand ischemia during cisplatin therapy.

    BACKGROUND: platinum is one of the most widely used agents in clinical oncology today. Serious toxic effects are well recognized. FINDINGS: To our knowledge, the current report describes the first case of severe allergic exfoliative dermatitis associated with ischemia and necrosis of the hands in a patient who had received multiple doses of this agent. We postulate that the tissue damage was caused by vasospasm of small vessels from the initial injury triggered by platinum or its associated immune complexes. CONCLUSION: platinum has become an integral part of combination chemotherapy for various solid tumors. Clinicians must recognize its toxic side effects and control them within tolerable limits.
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10/11. heparin-associated thrombocytopenia and thrombosis (HATT) presenting with livedo reticularis.

    BACKGROUND. heparin-associated thrombocytopenia and thrombosis (HATT) is an infrequently encountered syndrome characterized by ischemic necrosis of soft tissue and vital organs following anticoagulation with heparin. The syndrome is thought to be due to heparin-dependent platelet aggregation and thrombosis, which is mediated by pathologic immunoglobulins. CASE REPORT. A 60-year-old man developed truncal livedo reticularis and ischemic necrosis of the left foot associated with thrombocytopenia, disseminated intravascular coagulopathy (DIC), and microangiopathic hemolytic anemia during intravenous heparin therapy. skin biopsy from an area of livedo reticularis revealed fibrin thrombi in dermal blood vessels, which is characteristic of HATT. The diagnosis of HATT promoted discontinuation of heparin and a resulting rapid resolution of the livedo reticularis and hematologic abnormalities. No other potential causes of DIC were identified, and, other than stopping heparin, no specific therapy was employed. CONCLUSIONS. Periodic monitoring of platelets should be performed on all patients receiving treatment with heparin, as early detection of heparin-induced thrombocytopenia followed by discontinuation of the drug may prevent life threatening thrombotic complications. HATT should be included in the differential diagnosis of patients with livedo reticularis that occurs during heparin therapy.
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