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At least 253 records · Page 14Linked to original sources
PubMed1975

Friction blisters as a manifestation of pathomimia.

Self-inflicted skin lesions (pathomimia, artefacts) can be produced in a variety of ways, by the help of nails, razor blades, cigarettes, chemicals, etc. The present study reports three cases of pathomimia, in which the lesions consisted of vesicles or bullae producted by friction. Friction blisters can easily be produced in sites where the epidermis is both thick and firmly attached to the underlying tissues. The blisters have a characteristic histological appearance, which makes it possible to distinguish them from the blisters of different forms of vesicular and bullous diseases and from burn blisters which may also occur in pathomimia.

Adult↗
PubMed1984

Ketoconazole concentrations in human skin blister fluid and plasma.

To investigate ketoconazole penetration into skin, a single oral dose of 200 mg was administered to six healthy subjects. Plasma and cantharides blister fluid (CBF) levels were measured for 11 to 24 hours. In suction blister fluid (SBF) ketoconazole was determined 3, 6, and 9 hours after administration. Mean peak plasma levels of ketoconazole were found at 1 hour, they amounted to 3.03 +/- 0.55 micrograms/ml (n = 5). Apparent half-life of elimination was 1.8 hours. In cantharides blister fluid maximum ketoconazole concentrations were obtained at 6 hours being 1.05 +/- 0.32 micrograms/ml and declined rather slowly (half-life 4.2 hours; n = 3). Maximum concentrations in suction blister fluid were obtained 3 hours after administration (0.914 +/- 0.123 micrograms/ml). After 9 hours ketoconazole levels had declined to 0.216 +/- 0.044 micrograms/ml (n = 3). These concentrations exceed the ketoconazole concentrations proven to be effective in vitro up to 25 fold.

Adult↗
PubMed1978

Prostaglandins released into human burn blister fluid.

Acidic lipids were isolated from human burn blister fluid and the presence of prostaglandins E and F compounds was demonstrated by the thin-layer chromatography. Prostaglandins E1, E2 and F2alpha were identified and quantitatively determined by radioimmunoassay and by gas-liquid chromatography/mass spectrometry. Analyses on burn blister fluid obtained from 35 patients with skin burn indicated an extensive release of prostaglandins into the blister after burn injury in a few hours. The high levels of prostaglandins in burn blister fluid decreased gradually during 24 hours after burn.

Adolescent↗
PubMed1982

Bullous pemphigoid blister fluid stimulates eosinophil colony formation and activates eosinophils.

An eosinophil stimulating material (ESM) is described in the blister fluids (BF) of six patients with bullous pemphigoid (BP). This ESM is similar in function to a subspecies of human colony stimulating factor (CSF), CSF-alpha, since (i) it stimulated the production from bone marrow cells of day 14 colonies (31 +/- 15, arithmetic mean +/- 1 s.e.m. colonies, n = 5) in semi-solid agar, (ii) a large proportion (47 +/- 12%, n = 5) of these colonies were eosinophilic and (iii) it activated purified peripheral eosinophils as judged by increased autofluorescence (a mean increase of 23.6 +/- 6.6 units measured by flow cytometry, n = 10). BF from patients with four other blistering diseases, burn blisters, suction blisters from normal, eosinophilic or BP patients, various sera, histamine and eosinophil chemotactic factor (ECF-A) lacked activities in these assays. This description of a tissue accumulation of a CSF like substance suggests that there exists a physiological role for CSF in the periphery. In addition it supports the concept that local activation of eosinophils contributes to the pathogenesis of BP.

Aged↗
PubMed1995

Fracture blisters.

Fracture blisters can pose a problem when dealing with trauma. The potential to increase the complication rate, delay surgery, and prolong wound healing are possible sequelae. Edema has to be controlled, however, because the blisters can form in spite of ice, elevation, and compression. They may also appear even after prompt ORIF. High-energy trauma predisposes one to develop fracture blisters. Blisters can be discovered even after closed reduction and at a subsequent cast change. As with all pathologic conditions, the index of suspicion has to be high (Fig. 7).

Adult↗
PubMed1996

Induction of blister-causing antibodies by a recombinant full-length, but not the extracellular, domain of the pemphigus vulgaris antigen (desmoglein 3).

Pemphigus vulgaris (PV) is mediated by autoantibodies to desmoglein 3, the pemphigus vulgaris antigen (PVA). PVA and an extracellular domain of PVA-Ig fusion protein (PV-Ig) can completely adsorb the blister-causing Abs from PV patient sera, suggesting that the extracellular segment of PVA might be sufficient to induce pathogenic Abs. To test this, we immunized rabbits with either PVA or its extracellular domain (EPVA) expressed in insect cells in our laboratory. When Igs were passively transferred from these rabbits into neonatal mice, anti-PVA, but not the anti-EPVA, induced blisters. To understand the basis for their differential pathogenic effects, we examined the properties of these sera. Both sera showed comparable ELISA titers and indirect immunofluorescence reactivity against monkey esophagus, a source of native PVA. Moreover, EPVA, like PVA adsorbed blister-causing Abs from sera of PV patients and rabbits immunized with PVA. In contrast, when IgG preparations were incubated with fura-2-AM (acetyloxymethyl ester)-loaded human keratinocytes in culture, only IgG from anti-PVA serum induced intracellular calcium mobilization. These data showed that PVA but not EPVA can elicit Abs that induced blisters in neonatal mice and mediate intracellular signaling through calcium mobilization.

Amino Acid Sequence↗
PubMedDate not supplied

Plasma and skin blister fluid concentrations of metronidazole and its hydroxy metabolite after oral administration.

Plasma and cantharidin-induced skin blister fluid concentrations of metronidazole and its main metabolite-hydroxymetronidazole were determined after a single and multiple oral doses. Metronidazole is nitroimidazole compound applied for the treatment of Protozoa infections. It is also active against anaerobic bacteria. The maximum concentrations of unchanged drug and its metabolite following a single oral dose of 2 g were observed after 1 +/- 1 and 11 +/- 2 h in plasma, whereas in blister fluid after 6 +/- 2 and 16 +/- 5 h, respectively. The average ratio of area under concentration time curve (AUC) in blister fluid to that of plasma was 1.02 +/- 0.12 for parent drug and 1.02 +/- 0.02 for the metabolite. After multiple doses of metronidazole (0.25 g every 8 h) the concentrations of unchanged drug in plasma and blister fluid, collected before the morning dose and 2 h after its administration, exceeded the minimal inhibitory concentrations for majority of susceptible pathogens. Hydroxymetronidazole concentrations in body fluids at steady-state amounted to about 30-50% of the parent drug and they could contribute to the overall activity against susceptible microorganisms since antibacterial activity of the metabolite is about 30-65% that of the metronidazole.

Administration, Oral↗
PubMed2000

The shed ectodomain of collagen XVII/BP180 is targeted by autoantibodies in different blistering skin diseases.

Collagen XVII/BP180, an epidermal adhesion molecule, exists as a full-length transmembrane protein and as a soluble 120-kd ectodomain that is shed from the keratinocyte surface by furin-mediated proteolysis. Despite a number of studies on autoantibody targets in blistering skin diseases, it has remained unclear whether the physiologically shed ectodomain of collagen XVII plays a role as an autoantigen. Here we isolated the authentic, soluble form of human collagen XVII and showed that it is an autoantigen recognized by IgG and IgA autoantibodies in different blistering skin diseases and is, in some cases, the preferential target. The ectodomain was isolated from the epidermis, keratinocyte media, amniotic fluid, and pemphigoid blister fluid, and autoantibodies affinity-purified with this ectodomain bound to the proximal surface of the epidermis in normal skin but not in collagen XVII-deficient skin. The antibody reactivity was not dependent on the native conformation or the N-glycosylation of the soluble ectodomain, but was abolished by collagenase treatment. Sera of 81 patients with a clinically active blistering skin disease were reacted with full-length collagen XVII, the authentic soluble ectodomain, and recombinant fragments. In bullous and cicatricial pemphigoid, IgG reactive with full-length collagen XVII also recognized the soluble ectodomain. In linear IgA dermatosis and chronic bullous dermatosis of childhood, IgA targeted the soluble ectodomain more efficiently than the full-length protein. The use of recombinant fragments demonstrated that epitopes were present in several noncollagenous and collagenous subdomains of the molecule, and that a significant portion of the sera targeted Col15 domain, a hitherto unrecognized epitope region.

Adolescent↗
PubMed2000

Impact of pill organizers and blister packs on adherence to pill taking in two vitamin supplementation trials.

The impact of pill organizers on pill taking was determined in the Trial of Antioxidant Vitamins C and E (TRACE) Study, a factorial trial of vitamin C and vitamin E supplementation in 184 individuals. Participants were recruited in 1996-1997 and randomized to one of two groups (pill organizer or no organizer) and to one of four supplement groups for 2 months. The pill count (observed/expected X 100%) distribution was similar in the organizer and no organizer group for both vitamins. Mean differences in changes in serum vitamin levels between active and placebo groups did not differ by pill organizer use. The impact of pill organizers and blister packs was compared in another trial, the Vitamins, Teachers, and Longevity (VITAL) Study, in 297 individuals randomized in 1993-1994 to receive study pills either in blister packs or in pill organizers and to take one of two supplements. Among those with lower adherence, the pill count distribution in the blister-pack group exceeded that in the organizer group. Mean differences in serum vitamin E levels between active and placebo groups did not differ by types of pill packaging. In summary, use of blister packs, but not pill organizers, improved adherence as measured by pill counts among those with lower adherence. Neither pill delivery system improved adherence as measured by serum vitamin levels.

Aged↗
PubMed1989

Skin blister fluid levels of ketoconazole during repetitive administration in healthy man.

Ketoconazole administered orally is used in the treatment of superficial and deep mycoses. To evaluate its active concentrations in skin tissue, serum, suction blister fluid (SBF), and cantharides blister fluid (CBF) levels of total and non-protein bound ketoconazole were determined. In general, only the free drug is considered to be the active one. Six healthy subjects received 200 mg once daily for 5 days. Total ketoconazole concentrations were determined by HPLC. The unbound fractions of ketoconazole in SBF (2.3%) and CBF (1.2%) were calculated from plasma protein binding (99.0%). Before the ultimate dose, levels of unbound ketoconazole in SBF and CBF were 0.64 +/- 0.16 and 0.70 +/- 0.25 ng/ml and were thus in accordance with free ketoconazole serum levels (0.52 +/- 0.24 ng/ml; p greater than 0.05). Furthermore, following the ultimate dose, the areas under the blister fluid level-time curves of unbound ketoconazole did not differ from the respective areas under the serum level time curves, thus distribution equilibrium between serum and skin blister fluid was obtained. Peak concentrations of free ketoconazole were (SBF) 8.6 +/- 2.9 ng/ml and (CBF) 8.9 +/- 2.3 ng/ml. Free concentrations in SBF and CBF were far below the MIC values for dermatophytes and Candida ssp. reported in the literature, leaving the concentration-effect relationship of ketoconazole still open for discussion.

Adult↗
PubMed2005

The pathophysiology of autoimmune blistering diseases.

Knowledge of the pathophysiology of immunobullous diseases has been advanced by the demonstration that passive transfer of antibodies against skin autoantigens can induce blisters in experimental animals with clinical, histologic, and immunopathologic features similar to those seen in human patients. In this issue of the JCI, Liu et al. extend their earlier observations regarding an experimental murine model of bullous pemphigoid by showing that the plasminogen/plasmin signaling cascade synergizes with MMP-9 during the early phase of antibody-induced blister formation in vivo. In a separate study, Sitaru et al. show for the first time to my knowledge that passive transfer of experimental antibodies against type VII collagen create subepidermal blisters in mice that mimic those seen in patients with epidermolysis bullosa acquisita (see the related article beginning on page 870). While the articles by Liu, Sitaru, and their colleagues identify pathways of inflammation and tissue injury that, if interrupted, may abrogate blister formation, in a third study, Payne et al. utilized phage display technologies to isolate human anti-desmoglein monoclonal antibodies from a patient with pemphigus vulgaris and show that such antibodies have restricted patterns of heavy and light chain gene usage - findings suggesting that autoantibodies may represent an additional target for therapeutic interventions in patients with immunobullous diseases (see the related article beginning on page 888).

Animals↗
PubMed1994

Blistered: a gene required for vein/intervein formation in wings of Drosophila.

We have characterized the blistered (bs) locus phenotypically, genetically and developmentally using a set of new bs alleles. Mutant defects range from wings with ectopic veins and intervein blisters to completely ballooned wings where the distinction between vein and intervein is lost. Mosaic analyses show that severe bs alleles behave largely autonomously; homozygous patches having vein-like properties. Developmental analyses were undertaken using light and electron microscopy of wild-type and bs wings as well as confocal microscopy of phalloidin- and laminin-stained preparations. bs defects were first seen early in the prepupal period with the failure of apposition of dorsal and ventral wing epithelia. Correspondingly, during definitive vein/intervein differentiation in the pupal period (18-36 hours after puparium formation), the extent of dorsal/ventral reapposition is reduced in bs wings. Regions of the wing that fail to become apposed differentiate properties of vein cells; i.e. become constricted apically and acquire a laminin-containing matrix basally. To further understand bs function, we examined genetic interactions between various bs alleles and mutants of two genes whose products have known functions in wing development. (i) rhomboid, a component of the EGF-R signalling pathway, is expressed in vein cells and is required for specification of vein cell fate. rhove mutations (lacking rhomboid in wings) suppress the excess vein formation and associated with bs. Conversely, rho expression in prepupal and pupal bs wings is expanded in the regions of increased vein formation. (ii) The integrin genes, inflated and myospheroid, are expressed in intervein cells and are required for adhesion between the dorsal and ventral wing surfaces. Loss of integrin function results in intervein blisters. Integrin mutants interact with bs mutants to increase the frequency of intervein blisters but do not typically enhance vein defects. Both developmental and genetic analyses suggest that the bs product is required during metamorphosis for the initiation of intervein development and the concomitant inhibition of vein development.

Animals↗
PubMed2004

[A successfully treated case of a ruptured anterior wall aneurysm of the internal carotid artery (C2) which changed in form from blister-like to saccular type].

We successfully treated a case of ruptured anterior wall aneurysm of the ICA (C2) which changed in form from blister-like to saccular type. A 46-year-old woman developed subarachnoid hemorrhage on July 12, 2002. Cerebral angiogram demonstrated a blister-like aneurysm located in the left C2 portion of the internal carotid artery, but which didn't affect the arterial branches. Because of the risk of premature rupture during early surgery, delayed surgery was scheduled and the patient underwent serial study of the aneurysm. During 2 weeks of follow-up, the shape and size of the aneurysm changed in form blister-like to an enlarged saccular type aneurysm. On the day 18th, a left episubcombined approach, after insertion of a balloon catheter into the cervical ICA, was attempted and the aneurysm projecting antero-medially under the left carotid artery was exposed. The aneurysm had a distinct neck and its wall was not fragile. There was no macroscopic evidence of dissection of the ICA and the aneurysm was successfully clipped by conventional manipulation. Because of the difficulty in determining by angiographic evidence alone, whether an anterior wall aneurysm is a blister type or saccular type, careful follow-up is needed and if the shape or size changes, immediate appropriate treatment becomes mandatory. Intraoperative observation will determine the final diagnosis, as in this uncommon case.

Aneurysm, Ruptured↗
PubMed1978

Blister beetle poisoning in horses.

Case records of 21 horses with acute illness following ingestion of hay containing dead striped blister beetles (Epicauta spp) were selected for review. Abdominal pain, fever, depression, frequent urination, shock, and, occasionally, synchronous diaphragmatic flutter characterized clinical illness. Hematologic findings included hemoconcentration, neutrophilic leukocytosis, and hypocalcemia. Hematuria and low urine specific gravity were abnormal urinalysis results. Sloughing of the epithelium of the esophageal part of the stomach, hemorrhagic and ulcerative cystitis, enterocolitis, and myocardial necrosis were important post-mortem findings. Signs and lesions in 5 horses experimentally poisoned were similar to those of the natural disease. The findings were regarded as sufficiently characteristic of blister beetle poisoning to be useful in differential diagnosis but were not constant in all cases. Therefore, when blister beetle poisoning is suspected, access of affected horses to hay containing striped blister beetles should be demonstrated.

Animals↗
PubMed1981

Serum and blister fluid immune complexes in bullous pemphigoid: detection with C1q and monoclonal rheumatoid factor.

Eighty serum samples and 24 blister fluids from 51 patients with active bullous pemphigoid were tested for the presence of immune complexes by both a monoclonal rheumatoid factor (mRF) inhibition radioassay and a C1q-binding radioassay. Forty-two of the 80 serum samples were positive by the mRF assay, while 27 were positive by the C1q-binding assay. Antibody titres to the basement membrane zone did not correlate with levels of circulating immune complexes. Thirteen of 24 blister fluids had detectable immune complexes by the C1q assay, while only seven of 24 blister fluids were positive by the mRF assay. Sucrose density-gradient ultracentrifugation studies suggest that the mRF- and C1q-reactive substances in both bullous pemphigoid sera and blister fluids are of a size compatible with immune complexes. Although immune complexes are detectable in a high percentage of bullous pemphigoid patients, their role in this disease may be epiphenomenal rather than pathogenetic, merely reflecting the presence of autoantibody and soluble antigen.

Antigen-Antibody Complex↗
PubMed1996

Immune-mediated subepithelial blistering diseases of the mucous membranes. Improving the detection of circulating autoantibodies by the use of concentrated serum samples.

BACKGROUND AND DESIGN: Comparison of detection of circulating autoantibodies before and after concentration of serum samples from patients with suspected immune-mediated subepithelial blistering diseases of the mucous membranes. We determine whether the use of concentrated serum samples from patients with suspected immune-mediated subepithelial blistering diseases of the mucous membranes improves diagnostic sensitivity for circulating antibodies. We studied 13 patients from a university-based referral practice who had no skin lesions and a scarring subepithelial blistering disease of the mucous membranes. Three of these patients had detectable circulating autoantibodies and 10 had negative indirect immunofluorescence study results using standard techniques. The main outcome measures after concentration of serum samples were detection of circulating autoantibodies on salt-split skin by indirect immunofluorescence, immunoblotting, and immunoprecipitation. RESULTS: Of the 10 patients in whom circulating autoantibodies had not been detectable with standard techniques, circulating IgG antibodies were detected in 5 (50%) and circulating IgA antibodies in 3 (30%). Of the 3 patients in whom circulating autoantibodies had been detectable with standard techniques, 1 (33%) had circulating IgA antibodies that immunoblotted the 97-kd linear IgA bullous disease antigen only when concentrated serum samples were used. CONCLUSIONS: The use of concentrated serum samples can improve our ability to detect the presence and antigenic specificity of circulating autoantibodies in patients with suspected but unclassifiable immune-mediated subepithelial blistering diseases of the mucous membranes.

Autoantibodies↗
PubMed1978

Epidermal migration during the healing of suction blisters in rat skin: a scanning and transmission electron microscopic study.

Fluid-filled blisters, created on the skin of the inner surface of the pinna of heparinized rats by the application of suction, showed an intact basal lamina through which protruded hairs and remnants of hair follicles. The origin of epithelial cells and their spreading over the basal lamina were studied at intervals over 36 hours using scanning and transmission electron microscopy. The majority of epidermal cells arose from the outer root sheath of hair follicles and began to spread radially before 12 hours. By 36 hours the cells were confluent over most of the blister base. Inflammatory cells were few in number and rested mainly on the bare basal lamina rather than on the resurfacing cells. Some elongated epidermal cells showing tapering foot processes appeared to be migrating in from the epidermis at the edge of the blisters. The cells spreading from hair follicles were flat and polygonal. On these sheets of cells a few small folds and many filopodia were present at intercellular junctions and at the free margin of the leading cells. Large numbers of short microvilli covered the surface of some of the epidermal cells, especially at 24 and 36 hours; other epidermal cells were relatively smooth.

Animals↗
PubMed1989

Antagonism of the algesic action of bradykinin on the human blister base.

The effect of bradykinin (BK) and some analogues of BK on the human blister base was studied. BK produced reproducible dose-related increases in pain responses. A characteristic delay, which was not dose-related occurred between application of BK and the resultant response. The rank order of potency of several kinin analogues on the pain response was BK much much greater than sigma-cyclo-(Lys1-Gly6)-BK = sigma-cyclo-kallidin greater than des-Arg9-BK. No increase in pain response was seen with repeated application of the selective B1-receptor agonist des-Arg9-BK to the same blister base at 4h intervals. The B1 receptor antagonist des-Arg9-Leu8-BK was without effect against BK-induced responses. The B2-receptor antagonists, D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg-TFA and D-Pro-Phe-Arg-heptylamide produced significant antagonism of the bradykinin-induced pain responses at doses which had no effect against 5-hydroxytryptamine or potassium chloride. It is concluded that the kinin receptor mediating pain on the human blister base is of the B2 type.

Administration, Topical↗