Cases reported "Blister"

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1/8. Bullae and sweat gland necrosis after an alcoholic deep slumber.

    A 37-year-old man developed edematous areas and blisters on the right side of his face, chest, and arm after an alcoholic deep slumber. It was revealed that the affected body parts were those pressed during his alcoholic sleep. Histopathological findings of the patient's skin lesions showed typical sweat gland necrosis. serum enzyme level studies of aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and creatine phosphokinase were characteristic of muscular damage. This case report is an example of the typical findings of the effects of body pressure on soft tissue that can be seen in a dermatology clinic.
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2/8. coma blisters in a case of fatal theophylline intoxication.

    A case of fatal poisoning caused by theophylline toxicity (serum level 127 micro g/ml) is presented. At external examination, skin blisters on regions exposed to pressure were distinctive. Histologic examination demonstrated subepidermal bullae with eosinophilic necrosis of the eccrine sweat gland coil but no epidermal necrosis, vascular changes, or inflammatory infiltrate. To the authors' knowledge, this is the first description of coma blisters in a case of theophylline intoxication.
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3/8. Drug-induced sweat gland necrosis in a non-comatose patient: a case presentation.

    BACKGROUND: coma-induced bullae and sweat gland necrosis is a rare clinicopathological entity often associated with drug-induced coma. SUBJECT: We report a case with clinical and histopathologic findings characteristic of blisters and sweat gland necrosis occurring in a non-comatose patient. CONCLUSIONS: Skin blisters with underlying sweat gland necrosis is an entity previously reported to occur in comatose patients, our findings open new questions about the role of the drugs in the pathogenesis of those conditions.
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4/8. Bullous allergic hypersensitivity to bed bug bites mediated by IgE against salivary nitrophorin.

    In Central europe, bites from the common bed bug (Cimex lectularius) are nowadays rather uncommon. Nevertheless, infestations are sometimes observed in old framehouses and by immigration due to international travel and migration. The clinical picture of bug bites substantially varies between individuals, depending upon previous exposure and the degree of an immune response. The host immune response and potential protein antigens present in the saliva of C. lectularius or specific antibodies have not been characterized thus far. We describe a patient with bullous bite reactions after sequential contact with C. lectularius over a period of 1 year. In skin tests, we observed immediate reactions to the salivary gland solution of C. lectularius, which were followed by a pronounced partially blistering late-phase response. Immunoblot analysis of the patient's serum with salivary gland extracts and recombinant C. lectularius saliva proteins revealed specific IgE antibodies against the 32 kDa C. lectularius nitrophorin, but not to 37 kDa C. lectularius apyrase. Our data demonstrate that bullous cimicosis may be the late-phase response of an allergic IgE-mediated hypersensitivity to C. lectularius nitrophorin.
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5/8. Lack of long-term durability of cultured keratinocyte burn-wound coverage: a case report.

    Cultured epithelial autografts have been advocated for permanent closure of skin surfaces after massive thermal injuries. A 10-year-old boy sustained a nearly 100% total body surface area burn (98% full-thickness) in an explosion accident. Cultured epithelial autograft was used to cover 70% of the total body surface area on postburn day 26. In spite of early success of coverage, 60% of cultured epithelial autograft areas blistered and sloughed over the ensuing weeks. Electron microscopic examination of a biopsy specimen of the healed cultured epithelial autograft (80 days after placement) revealed a lack of dermal attachments of the anchoring fibrils. Additionally, blister fluid that was taken from the bullae of the cultured epithelial autograft revealed levels of 18 ng/ml thromboxane and 24 ng/ml prostaglandin E2. These levels are significantly higher than those seen in acute burn blister fluid and indicate an ongoing inflammatory process. Cultured keratinocytes, although they provide early wound closure, may not provide adequate long-term coverage for patients with massive burns.
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6/8. Occurrence of platelet-activating factor (PAF) and an endogenous inhibitor of platelet aggregation in diffuse cutaneous mastocytosis.

    We have identified PAF in the blister fluid from a patient with bullous mastocytosis, a rare form of mast-cell disease. We have found a novel endogenous inhibitor of platelet aggregation which obscured the presence of the PAF in unprocessed blister fluid and in ethanol or lipid extracts. The PAF was characterized by the demonstration of chromatographic, mass spectral and biological properties identical to those of authentic PAF. Thus this is the first demonstration of PAF in biological fluid from a patient with mastocytosis. High levels of immunoreactive prostaglandin d2 (PGD2) and histamine were also present in the blister fluid. The interaction between PAF and the inhibitor of platelet aggregation in patients with systemic mastocytosis may provide an explanation for some of the manifestations of the disease, in particular the episodic hypotension, cutaneous flushing and pallor.
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7/8. Localized subepidermal bullae after intravenous phenobarbital.

    The occurrence of subepidermal bullae and sweat gland necrosis in barbiturate-induced coma is well recognized. We report the case of a patient who received intravenous phenobarbital for refractory seizures and subsequently sustained subepidermal bullae without sweat gland necrosis in the skin around and proximal to the intravenous site. Although this may have been secondary to extravasation, a different mechanism of barbiturate-induced bulla formation may exist.
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8/8. immunoglobulins specific to mosquito salivary gland proteins in the sera of persons with common or hypersensitive reactions to mosquito bites.

    Using the immunoblot technique, we analyzed the quality and quantity of IgG, IgG4, and IgE specific to mosquito salivary gland (hereafter abbreviate as SG) components of aedes albopictus in the sera of volunteers with common reactions and of 3 patients with severe reactions. In the volunteers with delayed reactions only or with both delayed and immediate reactions, IgG against SG components of A. albopictus formed several faint or moderately stained bands. Those with immediate reactions showed several intense bands and many other weak bands. In volunteers, who had been bitten by aedes sp. frequently but had no skin reaction, and in severe cases, many intense IgG bands were observed. IgG4 bound to SG components were found in the sera of the common reaction group at the levels of 24 and 48 kD, but, in one severe case, no bands were observed, although the total IgG was very high. IgE levels specific to SG components were much higher in severe cases than in the volunteers. These results indicate that high titers of specific IgG and IgE and lack of IgG4 for particular components of SG may lead to severe allergic reactions in severe cases. immunoblotting analysis of the antibodies also verified the possibility of developing in vitro tests to identify causative species of the mosquito for severe cases.
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