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At least 217 records · Page 12Linked to original sources
PubMed1997

Assessment of postmortem blood alcohol concentrations by ethanol levels measured in fluids from putrefactive blisters.

It was the aim of the present study to investigate whether the postmortem blood alcohol concentration (BAC) can be assessed by means of ethanol values measured in fluids from putrefactive blisters. Fluids from one or two putrefactive blisters were collected in 45 putrefied corpses (postmortem interval: 3-23 days, graduation of the degree of decomposition into four stages) and compared with femoral vein blood or femoral muscle. Ethanol and so-called putrefactive alcohols were determined in all samples by double GC-measurements. The results were converted to the medium water content of blood of 80%. The investigations revealed a significant correlation between the ethanol values of femoral blood/muscle and putrefactive blister fluid (PBF) (r = 0.725, P < 0.001). With the exception of one case, PBF values of 0.11% or more (n = 11) corresponded to minimum blood/muscle concentrations of 0.085%; PBF values of more than 0.15% (n = 8) corresponded to blood/muscle levels of at least 0.159%. Regression analysis revealed the formula BAC (in %) = 0.785 X ethanol (PBF) +0.011. Relevant concentrations of putrefactive alcohols such as 1- and 2-propanol and l-butanol only occurred in cases with far advanced decomposition. Ethanol levels determined in fluids from different putrefactive blisters of the same body also demonstrated a significant correlation (r = 0.791, P < 0.001). Ethanol concentrations determined in PBF must be judged with caution, but PBF values > 0.15% point to corresponding blood levels with a high degree of probability, at least where advanced putrefaction is excluded.

Alcohol Drinking↗
PubMed2003

Production and resolution of cantharidin-induced inflammatory blisters.

While inflammatory blisters have long been utilized as a means of evaluating antimicrobial disposition to aid in the development of new treatments for skin and skin structure infections, sparse data are available regarding the healing of the blisters once the experiment has been completed. We report the blister induction technique and resolution time in ten volunteers enrolled in a pharmacokinetic study using the cantharidin-induced inflammatory blister technique.

Anti-Bacterial Agents↗
PubMed2004

The miscellaneous blistering disorders.

Historically, the classification of the blistering disorders has been arbitrarily assigned by common clinical features (ie, vesicle, bullae), etiologic factors (ie, infectious, immunologic), or histologic parameters (ie, intraepidermal and subepidermal). There are distinct advantages to each of these classification systems, yet there remain a small number of either common conditions that rarely manifests as a blistering disorder or uncommon conditions that routinely blister, defying conventional classification. Such misfits comprise a miscellaneous group of blistering conditions that merit special consideration.

Bites and Stings↗
PubMed2001

Bullous amyloidosis: the mechanism of blister formation revealed by electron microscopy.

BACKGROUND: Few electron microscopic studies of blister lesions in bullous amyloidosis have been reported, and the mechanism of blister formation remains to be elucidated. This study was designed to examine the nature of bullous amyloidosis ultrastructurally, and clarify the pathogenesis of blister formation. METHODS: We examined a 47-year-old woman with IgD-lambda type myeloma, suffering from bullous lesions on her hands and feet caused by trauma or rubbing. Light and electron microscopic studies were performed. RESULT: Ultrastructurally, amyloid deposits aggregated under the lamina densa. Keratinocyte protrusions penetrated the dermis through the gap in the lamina densa and enfolded amyloid deposits. Amyloid globules were found in enlarged intercellular spaces of keratinocytes. Desmosomes were sparsely distributed in some areas of the epidermis. CONCLUSION: These results indicate that keratinocytes enfold the amyloid globules and take them in the intercellular space of epidermis, and that the breakdown of the lamina densa and widening of the intercellular space between keratinocytes induce skin fragility. Trauma or rubbing of her hands and feet appears to act as the localized precipitating factor of blister formation in bullous amyloidosis.

Amyloid↗
PubMed2006

Synergistic pathogenic effects of combined mouse monoclonal anti-desmoglein 3 IgG antibodies on pemphigus vulgaris blister formation.

Pemphigus vulgaris (PV) is an autoimmune blistering disease caused by anti-desmoglein 3 (Dsg3) IgG antibodies. Previously, we generated an active mouse model for PV by adoptive transfer of splenocytes from immunized or naive Dsg3(-/-) mice. In this study, we isolated 10 anti-Dsg3 IgG mAbs (NAK-series) from PV model mice generated by transfer of naive Dsg3(-/-) splenocytes. We characterized their epitopes using domain-swapped and point-mutated Dsg1/Dsg3 molecules and examined their pathogenic activities in blister formation in three different assays. In a passive transfer model using neonatal mice, eight of 10 NAK mAbs showed pathogenic activity when injected together with half the minimum pathogenic dose of anti-Dsg1 IgG autoantibodies from pemphigus foliaceus (PF) patients. None of the mAbs could induce the PV phenotype when individual hybridoma clones were inoculated by peritoneal injection into adult Rag2(-/-) mice. NAK mAbs displayed a range of potency in an in vitro dissociation assay using primary cultured mouse keratinocytes. Interestingly, when multiple hybridoma clones recognizing different epitopes were inoculated in combination, recipient mice developed the PV phenotype. In vitro dissociation assays confirmed that combined NAK mAbs had synergistic pathogenic effects. These findings indicate that although an individual anti-Dsg3 IgG is not sufficient to cause blistering in adult mice, several together can induce the PV phenotype. These mAbs will provide a valuable tool to investigate the molecular mechanisms of blister formation, mimicking the effects of the polyclonal IgG antibodies found in patients.

Aging↗
PubMed2000

Human anti-laminin 5 autoantibodies induce subepidermal blisters in an experimental human skin graft model.

Patients with one form of cicatricial pemphigoid have IgG antibasement membrane autoantibodies against laminin 5 (alpha3beta3gamma2). Although passive transfer of rabbit anti-laminin 5 IgG to neonatal mice has been shown to induce subepidermal blisters that mimic those in patients, it has not been possible to directly assess the pathogenic activity of human autoantibodies in this animal model because the latter do not bind murine skin. To address this question, a disease model in adult mice as well as SCID mice bearing human skin grafts was developed. Adult BALB/C mice challenged with rabbit anti-laminin 5 IgG developed, in a concentration-related fashion, erythema, erosions, and crusts surrounding injection sites, histologic evidence of noninflammatory, subepidermal blisters, and deposits of rabbit IgG and murine C3 in epidermal basement membranes. Anti-laminin 5 IgG also induced subepidermal blisters in: adult complement-, mast cell-, and immuno-deficient mice; adult BALB/C mice pretreated with dexamethasone; and human skin grafts on SCID mice. Alterations did not develop in matching controls challenged with identical amounts of purified normal rabbit IgG or bovine serum albumin. Using this adult mouse model, human skin grafts on SCID mice were challenged with purified IgG from patients with alpha subunit-specific, anti-laminin 5 autoantibodies, or normal controls. Patient (but not control) IgG induced epidermal fragility as well as noninflammatory, subepidermal blisters in grafted human (but not adjacent murine) skin. Moreover, whereas all mice that received patient autoantibodies had anti-laminin 5 IgG in their circulation, deposits of human IgG were present only in the epidermal basement membranes of grafts. Interestingly, these in situ and circulating autoantibodies were predominately of the IgG4 subclass. These studies demonstrate that human anti-laminin 5 autoantibodies are pathogenic in vivo and describe an animal model that can be used to define disease pathomechanisms and biologically important domains within this autoantigen.

Animals↗
PubMed2002

Increased interleukin 10, tumor necrosis factor alpha, and interleukin 6 levels in blister fluid of toxic epidermal necrolysis.

BACKGROUND: Toxic epidermal necrolysis is a severe, usually drug-induced disease that shares clinical, histologic, and immunologic similarities with the severe forms of cutaneous acute graft-versus-host disease. OBJECTIVE: Our purpose was to further characterize common immune-inflammatory pathways in these skin disorders by measurement of different cytokines. METHODS: Evaluation of serum levels of interleukin 10 (IL-10), tumor necrosis factor alpha, IL-6, and soluble IL-6 receptor in the early phase of both diseases and in blister fluid of toxic epidermal necrolysis. RESULTS: Serum levels of IL-10 and IL-6 were significantly higher in patients with toxic epidermal necrolysis (P =.0001) and acute graft-versus-host disease (P =.001) compared with those of blood donors. We found an increase in IL-6 levels in blister fluid and significantly higher levels of IL-10 (P =.018) and tumor necrosis factor alpha (P =.028) in blister fluid compared with serum in patients with toxic epidermal necrolysis. CONCLUSION: A similar serum cytokine profile of toxic epidermal necrolysis and acute graft-versus-host disease further emphasizes common immunologic mechanisms. The presence of inflammatory cytokines, IL-6 and tumor necrosis factor alpha, in the blister fluid of patients with toxic epidermal necrolysis is associated with significantly higher levels of IL-10, which through its down-regulatory role, may be involved in limitation of the disease extension.

Adolescent↗
PubMed1986

Blistering diseases in children. How to recognize and treat the most common.

The most common blistering diseases encountered in children are impetigo, burns, acute dermatitis, friction blisters, viral blisters, insect bite reactions, and linear IgA dermatosis. Diagnosis should be based on specific clinical manifestations and, when necessary, results of a Tzanck test or skin biopsy. A search for an intact blister is always warranted when erosions, oozing, or crusts are noted.

Acute Disease↗
PubMed1984

The pharmacokinetics of ceftriaxone in serum, skin blister and thread fluid.

Following 4 g of ceftriaxone, given intravenously, to eight volunteers, the antibiotic concentration in serum, suction skin blister fluid and fluid from subcutaneously implanted threads was followed for 28 h. High and sustained levels were found in both serum and extravascular fluids; the mean maximum serum concentration was 448 mg/l, and the mean peak concentrations in blister and thread fluid were 94 mg/l and 63 mg/l, respectively. The terminal, half-lives were: serum 7.2 h, blister fluid 10.3 h and thread fluid 11.3 h. The total area under the concentration versus time curves for serum was 1636 mg X h/l. For blister and thread fluid the areas were 1573 mg X h/l and 808 mg X h/l. The results suggest a twice daily dosage regimen.

Adult↗
PubMed1986

Early protein alteration in blister fluid and serum associated with burn injury.

Since the most common site of infection in burned patients is the burn wound, we have previously studied the biologic effect of burn wound blister fluid (BF) on control lymphocyte and neutrophil activity. BF will not support the phagocytosis of Pseudomonas by normal neutrophils, and a subset of the BF samples suppressed the maximal mitogen response of control lymphocytes by more than 50%. The current work was carried out to analyze in depth the composition of BF using crossed immunoelectrophoresis. Twenty BF and six serum specimens collected from 20 patients between 6 and 18 hours postburn had 19 separate proteins measured. These proteins included immunologic proteins, antiproteases, acute-phase reactants, carrier proteins, and lipoproteins. A total of 546 protein measurements were made. The concentrations of all subgroups of proteins were significantly lower in the BF and burn serum specimens than in control serum. When the blister fluids were stratified according to their effect on normal lymphocyte activity, the suppressive blister fluid samples had higher levels of C3 and lower levels of I alpha I than the nonsuppressive samples. The elevation in C3 was secondary to the local activation of C3 and the generation of multiple C3 breakdown products. These changes in C3 are of potential biologic importance, since evidence has accumulated indicating that the various fragments of C3 can modulate both neutrophil and lymphocyte function. Thus, the results of this study suggest that local changes in the blister fluid may adversely affect local immunity and predispose the patient to burn wound sepsis.

Adolescent↗
PubMed1976

The blister and the second degree burn in guinea pigs: the effect of exposure.

A reproducible partial-thickness burn was inflicted on 100 albino guinea pigs. With the blister intact, the evaporative water loss from the burn surface was essentially the same as from normal unburned skin. When the blister was removed, the rate of water loss was initially more than 100 times normal, and it remained 20 to 50 times the normal rate throughout the first week. This high rate of water loss was associated with an increasing depth of wound destruction (from dehydration) and a thickening of the overlying crust. Microscopic examination showed that previously viable dermis was incorporated in this crust. The depth of dermal loss was negligible when the blister was left intact, and improved healing resulted. We believe it is important to leave burn blisters intact, whenever possible.

Animals↗
PubMed1982

Ultrastructure of blister formation in epidermolysis bullosa hereditaria: V. Epidermolysis bullosa simplex localisata type Weber-Cockayne.

The ultrastructure of epidermolysis bullosa simplex type Weber-Cockayne has as yet not been studied systematically. Therefore biopsies of blisters freshly produced by friction after a hot bath were investigated by electron microscopy in 8 subjects of 6 families. Blister formation was found always to start in the basal layer of the epidermis. At first the cytoplasm with the cell organelles appears to become diluted, then holes develop in the cytoplasm which merge and finally form cytolytic blisters between the dermo-epidermal junction and the nucleus. The cell organelles remain remarkably intact. The cause of blister formation is still unknown, however, no structural abnormality was observed.

Adolescent↗
PubMed1986

Determination of anaphylatoxin concentrations in suction blisters in patients with psoriasis.

Concentrations of C3a and C4a anaphylatoxins in suction blister fluids were determined by radioimmunoassay in patients with psoriasis and normal controls. Comparison of anaphylatoxin levels between serum samples and blister contents in the same subjects revealed that the levels of both C3a and C4a anaphylatoxins were significantly higher in the former than the latter even in those raised on normal skin, suggesting that the classic complement pathway is activated during suction procedure. Therefore we cannot regard suction blister fluid to be simply representative of undisturbed interstitial tissue fluid as far as the complement system is concerned. There was no difference in anaphylatoxin levels between those from uninvolved skin of psoriatic patients and those from normal controls. However, significantly high anaphylatoxin levels were noted in fluids of suction blisters raised on lesional skin as compared with those produced on uninvolved skin in psoriatic patients.

Adolescent↗
PubMed1980

Evaluation of cellular injury in skin utilizing enzyme activities in suction blister fluid.

Suction blisters were produced on the skin of anesthetised rats and marker enzyme activities measured in the blister fluid from normal and chemically damaged skin. Cutaneous application of tributyltin, in doses known to produce morphological damage, increased the activity of a number of enzymes in the blister fluid within 2.5 hr. The increases were dose-related and resulted from cutaneous damage as they were detected at times and doses when there were no comparable changes in plasma enzyme activities. Increased enzyme levels in suction blister fluid from chemically damaged skin appear to reflect the degree of skin injury and may offer a direct and quantitative assessment of this injury.

Acetylglucosaminidase↗
PubMed1997

Prolidase activity in chronic wound and blister fluids.

We investigated prolidase activity in samples derived from wound fluid as well as blister fluid. Prolidase activity was elevated in fluid samples collected from wounds over the levels in sera collected from patients with chronic wounds (P < 0.05). Prolidase activity was also present in samples taken from blister diseases. However, prolidase activity in blister fluid was not higher than that in sera collected from patients with blister diseases. Our results indicate that prolidase may play a role in wound healing.

Adult↗
PubMed1977

Rapid blister formation in human skin with ammonium hydroxide.

The topical application to human skin of a 1:1 aqueous solution of ammonium hydroxide in a well drilled into a plastic block will provoke an intra-epidermal blister in an average time of about 13 min. The blister roof can be used for physico-chemical analyses of the horny layer while the base is suitable for studies of wound healing, bacterial infections, etc. The minimal blistering time (MBT) increases directly as the number of cell layers of the stratum corneum and ranges from 3 to 57 min in different regions and persons. The intensity of the dermatitis provoked by a 24 h exposure to sodium lauryl sulphate is strongly correlated with the MBT. The latter is therefore a reliable measure of cutaneous irritability. The blisters are virtually painless. The inflammatory reaction clinically and histologically is slight. Healing is rapid without scarring.

Adolescent↗
PubMed1978

Acid hydrolases in blister fluid. I. Characterization and quantification of acid phosphatase.

Acid phosphatase has been characterized and quantified in human suction blister fluid, interstitial fluid and serum. The acid phosphatases of suction blister fluid and serum showed differences in their pH activity curves, Michaelis-Menton constants, heat stabilities and sensitivities to inhibition by tartrate and fluoride. The behaviour of the interstitial fluid enzyme was intermediate between these two. The levels of activity in blister fluid and serum were very similar, both being more than twice that of interstitial fluid. These results suggest that the acid phosphatase activity in suction blister fluid is derived largely from the overlying epidermis rather than from serum.

Acid Phosphatase↗
PubMed1980

Cellular events leading to blister formation in bullous pemphigoid.

Cellular events occurring in eight patients with bullous pemphigoid were studied by light and electron microscopy. Sections (0.5 micrometer) of large surface area, overlapping blisters and surrounding skin, were examined and correlated ultrastructural studies were performed on selected areas. The peroxidase contained in granules of neutrophils, eosinophils and young macrophages was visualized by incubation with diaminobenzidine and hydrogen peroxide. This cytochemical reaction was used as a marker to study the release of granule enzymes from these inflammatory cells. The release of such enzymes from eosinophils and occasionally from macrophages on the epidermal basement membrane (more precisely in the lamina lucida) was demonstrated in the skin surrounding the blisters in four patients. The release of these enzymes was also observed in the floor of the blisters in all eight patients. It is well known that these granules contain several proteolytic enzymes. These observations are therefore consistent with the proposal that proteolytic enzymes of eosinophils play a pathogenic role during the initial stages of blister formation in bullous pemphigoid.

Blister↗