1/11. 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.- - - - - - - - - - ranking = 1keywords = sweat gland, sweat, gland (Clic here for more details about this article) |
2/11. 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.- - - - - - - - - - ranking = 0.2keywords = sweat gland, sweat, gland (Clic here for more details about this article) |
3/11. 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.- - - - - - - - - - ranking = 1.4keywords = sweat gland, sweat, gland (Clic here for more details about this article) |
4/11. Blisters, ulceration and autonomic neuropathy in carpal tunnel syndrome.We describe three patients with trophic ulceration and blistering of the fingertips associated with carpal tunnel syndrome. One of the patients also had non-insulin-dependent diabetes mellitus. Autonomic neuropathy distal to the carpal tunnel was probably present in all subjects at the time of presentation; in the patient with recent symptoms the skin was warm, and sweating was virtually absent, whilst the other two patients described cold skin, consistent with prolonged autonomic neuropathy.- - - - - - - - - - ranking = 0.013024223147575keywords = sweat (Clic here for more details about this article) |
5/11. Histopathological and ultrastructural study of ectodermal dysplasia/skin fragility syndrome.ectodermal dysplasia/skin fragility syndrome (EDSFS) (MIM604536) is a newly described autosomal recessive disorder characterized by skin fragility and blistering, palmoplantar keratoderma, abnormal hair growth, nail dystrophy, and occasionally defective sweating. It results from mutations in the PKP1 gene encoding plakophilin 1 (PKP1), which is an important component of stratifying epithelial desmosomes and a nuclear component of many cell types. Our study was performed to further characterize the histopathology of EDSFS in different cutaneous sites with a special emphasis on the hypotrichosis and keratoderma. A total of 4 biopsies were obtained from 2 EDSFS female patients, aged 9 days to 4 years. The biopsies were taken from the blistering skin of the leg and trunk, the hyperkeratotic skin of the sole, and the hypotrichotic scalp. The observed histopathologic features included: widened intercellular spaces, suprabasal intraepidermal clefts and blisters with acantholytic keratinocytes, detachments of the upper epidermal layers due to disadhesion, varying degrees of dyskeratosis that were much more pronounced in the plantar hyperkeratotic skin, and increased number of catagen-telogen hair follicles. The electron-microscopic observations attributed the disadhesion and acantholysis to reduced numbers of small hypoplastic desmosomes, and the dyskeratosis to the detachment of intracellular keratin filaments from the desmosomes with perinuclear condensation, which might also underlie the plantar keratoderma. The hair follicle findings suggest disturbance in the hair cycle, which might be attributed to disturbed nuclear PKP1 function or result from aberrant desmosomal signaling.- - - - - - - - - - ranking = 0.013024223147575keywords = sweat (Clic here for more details about this article) |
6/11. 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.- - - - - - - - - - ranking = 0.00065095358703385keywords = gland (Clic here for more details about this article) |
7/11. 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.- - - - - - - - - - ranking = 0.00032547679351693keywords = gland (Clic here for more details about this article) |
8/11. coma blisters: report and review.coma blisters are self-limited lesions that occur in the setting of coma of various causes, but are most commonly associated with barbiturate overdose. Examination of a skin biopsy specimen demonstrates the characteristic presence of eccrine sweat duct necrosis. Although the exact cause of coma blisters remains unknown, they are not related to underlying infections or rheumatologic disorders, and do not contraindicate the continued therapeutic use of barbiturates.- - - - - - - - - - ranking = 0.013024223147575keywords = sweat (Clic here for more details about this article) |
9/11. 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.- - - - - - - - - - ranking = 0.00032547679351693keywords = gland (Clic here for more details about this article) |
10/11. 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.- - - - - - - - - - ranking = 0.4keywords = sweat gland, sweat, gland (Clic here for more details about this article) |
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