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At least 127 records · Page 7Linked to original sources
PubMed1986

Elevated levels of human collagenase inhibitor in blister fluids of diverse etiology.

Blister fluids from a variety of bullous disorders were examined for the presence of human collagenase inhibitor. A protein immunologically identical to the collagenase inhibitor produced by human skin fibroblasts was found in high concentrations within bullae of diverse etiologies. Levels of collagenase inhibitor in blister fluids ranged from 0.9-12.5 micrograms/ml, averaging 4.9 micrograms/ml. The mean values were 3- to 4-fold greater than those present in the sera of corresponding patients and exceeded plasma levels by 6- to 8-fold. The time course of collagenase inhibitor accumulation in blister fluid was studied using heat- and suction-induced bullae. The concentration in newly formed blisters was approximately 0.5 micrograms/ml, virtually identical to plasma inhibitor levels, and remained constant for approximately 4 h. Inhibitor concentrations then rose rapidly, reaching peak values of approximately 6 micrograms/ml after 48 h. We speculate that the role of this inhibitor in blister fluid involves the inhibitions of active proteinases within the bulla cavity and may occur to limit the extent of blister formation or to assist in wound repair.

Adult↗
PubMed1979

The determination of lipids and proteins in suction blister fluid.

The concentration of 5 different proteins in suction blister fluid and serum was determined by immunotechniques. These proteins, varying in size and molecular weight (6,600-2,300,000) were insulin, albumin, high density lipoprotein determined as apoprotein A-I, alpha 2-macroglobulin and low density lipoprotein measured as apoprotein B. The difference in the blister fluid/serum concentration ratio of the proteins was dependent on the molecular weight and followed mainly the law of diffusion. Moreover, the amounts of insulin, albumin and apoproteins A-I and B in suction blister fluid were the same as those reported in peripheral lymph. The results indicate that the sieve function of the capillary basement membrane remains intact during the formation of the suction blisters. Suction blister fluid might therefore be regarded as representative of interstitial fluid. The concentrations of 4 different lipids (cholesterol, cholesterolesters, triglycerides and phospholipids) were also determined and their blister fluid/serum concentration ratio proved to have a fairly constant value of 0.25.

Blister↗
PubMed1980

Eosinophil chemotactic factor (ECF) in blister fluid of dermatological diseases.

The occurrence of low molecular weight (less than 500 dalton) eosinophil chemotactic factor (ECF) was studied in the blister fluid of patients with various dermatological diseases by an in vitro chemotaxis method. After chromatographic separation of the test substance on a small Sephadex G 25 column, ECF was demonstrated in blisters of five patients with bullous pemphigoid, in three patients with systemic drug reactions and in one patient with blisters are contact with primula. ECF was not found in blisters of patients with epidermolysis bullosa and herpes gestationis or in DNCB-induced blisters. Fluid obtained from suction blisters was negative in normal controls and in unaffected skin of patients with atopic eczema, but contained ECF in eczematous areas. The demonstration of ECF in tissue fluid suggests that this factor plays a role in the local accumulation of eosinophils at sites of certain inflammatory reactions.

Blister↗
PubMed1986

Proteolytic enzymes in blister fluids from patients with dermatitis herpetiformis.

Proteolytic enzymes may be involved in blister formation in dermatitis herpetiformis (DH). We have examined collagenase, gelatinase and elastase-like enzyme activities in fluids collected from spontaneous blisters and from suction blisters raised on developing DH-lesions induced by application of potassium iodide. Control suction blisters were raised on unaffected DH-skin and on healthy volunteers. High enzyme activities were found in spontaneous blisters, and suction blister fluids obtained from developing lesions showed increased levels of gelatinase and elastase-like enzymes. Inhibitor studies revealed that a part of the elastase-like enzyme activity might be derived from inflammatory cells. Gel filtration chromatography disclosed two separate elastase-like enzymes which, as they had high molecular weights, could be either enzyme-inhibitor complexes or aggregates.

Blister↗
PubMed1982

The healing of suction blisters in pig skin.

The healing of intact suction blisters in pig skin was studied using fluorescein-labelled lectins as well as conventional histological techniques. After blistering, initially overt separation was observed at the dermo-epidermal junction, but the separated epidermis appeared to re-attach within 9 h. Massive infiltration of the dermis and the epidermis by inflammatory cells, including eosinophils, was observed. By day 4 focal detachment of the epidermis occurred spontaneously, and towards day 9 the appearance of the blistered areas had almost returned to normal, apart from isolated patches of thin epidermis devoid of rete ridges. It is proposed that the sloughing the of the epidermis on day 4 is related to the presence of inflammatory cells and that the restoration of normal dermo-epidermal relations is dependent on the basement membrane zone remaining intact. The secondary blistering seen in day 4 specimens and the inflammatory cell involvement are in many ways similar to the blistering processes observed in certain human cutaneous disorders, such as dermatitis herpetiformis and bullous pemphigoid, and therefore suction blisters in pig skin might provide a suitable animal model for these diseases.

Animals↗
PubMed1981

Fluxes, junctions, and blisters in cultured monolayers of epithelioid cells (MDCK).

The formation of blisters is a transient phenomenon that led Dr. Leighton to describe its observation with time-lapse photography in the MDCK monolayer to a "gently boiling oatmeal." One may ask why is it transient and why most areas are momentarily not blistering. The observations discussed in this article indicate that (a) at the blister, junctions are really tight; (b) when transported fluid is allowed to escape through a permeable support, junctions are also tight, but (c) when the support is impermeable the junctions allow ouabain and peroxidase through. This suggests that, if the attachment of the monolayer is strong enough, the accumulation of fluid (Figure 7) bursts the junctions. If, on the contrary, junctions withstand the pressure, factor 3 of Figure 7 prevails over the others, and a blister is formed. In all the rest of the monolayer junctions seem to be open. This is in keeping with the observation by Rabito et al.,27 that if the monolayers are prepared on weakened supports, blisters are much bigger than under control conditions. It also allows the measurement of ionic fluxes and labeling of pumping sites at the basolateral membrane. As a corollary, one may say that some of the factors known to affect blistering 26 may very well act through modifications in the occluding junctions.

Animals↗
PubMed1991

Interface-area-to-volume ratio of interstitial fluid in humans determined by pharmacokinetic analysis of netilmicin in small and large skin blisters.

Human pharmacokinetics of netilmicin during multiple dosing were studied in serum and in the fluid of skin blisters with two different ratios of interface area to fluid volume. The kinetics in the blisters followed the serum concentration-time curve with a delay but with a similar elimination half-life of 2.4 h. The kinetics in the 40-microliters blisters followed closely the theoretically calculated concentrations of the peripheral compartment of a two-compartment model. In contrast, the concentrations in the 120-microliter blisters increased less rapidly, lower peaks were achieved, and concentrations decreased with a significantly longer delay. A very similar area-specific flow or clearance rate of 1.6 microliters.h-1.mm-2 was calculated for the interface area between the serum compartment and either the small or large blisters. The observed rapid mass transfer between serum and blister fluid suggests similar oscillations of concentrations in serum and in small interstitial fluid compartments.

Adult↗
PubMed2006

Primary treatment of a blister-like aneurysm with an encircling clip graft: technical case report.

OBJECTIVE: Blister-like aneurysms at nonbranching sites in the supraclinoid portion of the internal carotid artery are a rare but important cause of subarachnoid hemorrhage. We report a case of subarachnoid hemorrhage caused by a ruptured blister-type aneurysm, review the pertinent literature, and hope to remind readers of the wisdom of the use of an encircling clip as the primary treatment of these challenging lesions. CLINICAL PRESENTATION: A 41-year-old woman presented with sudden onset of headache. An admission computed tomographic (CT) scan revealed thick and diffuse subarachnoid hemorrhage involving primarily the carotid cistern and the proximal left sylvian fissure. A cerebral angiogram was initially interpreted as absent for aneurysm, but a follow-up angiogram performed 1 week later confirmed an enlarging aneurysm. INTERVENTION: A craniotomy with placement of an encircling clip graft around a blister-like aneurysm was performed. CONCLUSION: Although Sundt advocated the encircling clip graft for the blister-type aneurysm almost 40 years ago, use of an encircling clip graft in the treatment of blister-like aneurysms of the supraclinoid portion of the internal carotid artery seems to be reserved as a secondary or "rescue" measure in current practice. Neurosurgeons must familiarize themselves with this distinct entity (the blister-type aneurysm), recognize the possible risks associated with parallel clipping, and consider the use of an encircling clip graft as the primary treatment.

Adult↗
PubMed2000

The association of blisters with musculoskeletal injuries in male marine recruits.

A prospective study examining the epidemiology of blisters and, in particular, the association of blisters with subsequent injuries was conducted involving 2,130 male US Marine Corps recruits participating in initial physical training at the Marine Corps Recruit Depot in San Diego, California. From January 1993 through September 1994, recruits experienced an incidence of 2.05 blisters per 100 recruit-months. Recruits with blisters were 50% more likely to experience an additional training-related injury. Blisters, in combination with other related injuries, resulted in 159 clinic visits, 103 days of assigned light duty, and 177 lost days of training. This loss of time cost a minimum of $29,529. Extrapolating to the annual population of recruits, this represents an approximate annual expense of $690,000. Aggressive blister prevention and management in this setting has the potential to greatly reduce morbidity and fiscal costs.

Absenteeism↗
PubMed2004

Tape blisters that develop after hip fracture surgery: a retrospective series and a review of the literature.

A tape blister, a skin excoriation that occurs under the taped portion of surgical bandages, can be a source of postoperative morbidity. Tape blisters are caused by the separation of the epidermis from the dermis at the dermal-epidermal junction. Tape resistant to stretching contributes to blister formation because of the concentration of forces at the ends of the tape. Although tape blisters are a pervasive clinical problem, their incidence after hip surgery has rarely been reported in the orthopedic literature. Therefore, we retrospectively reviewed a consecutive series of patients with hip fractures to determine the incidence of tape blisters at our institution. One hundred three patients were included in the study. Tape-related injuries occurred in 22 patients (21.4%). Patient age, patient sex, number of medical comorbidities, smoking history, nutritional status, and type of surgery were not statistically significantly associated with risk for developing tape blisters.

Anti-Infective Agents, Local↗
PubMed1991

[Bacteriological investigation of burn blister fluid].

Under a sterilized technique the fluid of the unbroken blister was obtained for bacterial culture in 73 burned patients with different ages (5 months-67 Y) and extent of injury (1.5%-96% TBSA). Bacterial count was carried out if a positive result is obtained. Among the 73 patients, positive cultures were observed in 12, an incidence of 16.4%. Patients suffering from serious or extremely serious thermal injuries showed a positive culture rate of 15%. Bacterial count of the blister fluid appeared to be higher in patients with extensive burns. Most of the bacteria were common resident organisms of the human body. Of the 4 patients with their blister fluid bacteria counts over 2000 CFU/ml, 2 died from sepsis, while 8 patients with lower than 2000 CFU/ml bacteria in their blister fluid survived. The results suggested that large number of bacteria in the blister fluid might further depress local immunity, so that the patient is more susceptible to infections. It is therefore suggested that culture of blister fluid and bacterial count should be done immediately in the extensively burned patient just after admission.

Adolescent↗
PubMed1978

Transfer of penicillin G and ampicillin into human skin blisters induced by suction.

The antibiotic concentrations in untreated and endotoxin-treated suction blisters was studied in 15 healthy adults. In a pilot study, 2 mega units of penicillin G were given as an intravenous bolus injection to two subjects. For further studies, a single dose of 800 mg bacampicillin was given orally to 13 individuals. The penicillin G concentrations in the blister fluid were highest approximately 15 minutes after the dose, and exceeded that of serum after 1.5 hours. With ampicillin the blister fluid concentration reached maximum levels after approximately 2 hours, were equal to serum levels after 3 hours, and were later persistently in excess of serum levels. The ampicillin half-life was 136 and 100 minutes in the two types of blister fluid, as compared to 65 minutes for serum. A marked differences between the antibiotic concentrations in inflammatory and non-inflammatory blisters was seen in the pilot study with penicillin G. However, in the experiments with bacampicillin, no significant difference was demonstrated. This suction blister technique appears to be a useful method for studies on extravascular antimicrobial activity in man.

Adult↗
PubMed1988

[Transfer of injected sulbactam/cefoperazone into burn blister fluid].

Transfer of sulbactam/cefoperazone (SBT/CPZ) into the burn blister fluid was studied in 10 burn patients after one shot intravenous injection of 50 mg/kg SBT/CPZ (CPZ 25 mg/kg, SBT 25 mg/kg). CPZ and SBT concentrations in serum and burn blister fluid were determined using bioassay and high performance liquid chromatography (HPLC). The concentration of CPZ in serum reached 109.5 +/- 9.2 micrograms/ml (mean +/- S.E.) at 0.25 hour after injection, and decreased to 6.8 +/- 2.3 micrograms/ml after 8 hours. The concentration of CPZ in burn blister fluid peaked at 4 hours and reached 28.2 +/- 8.0 micrograms/ml. The concentration of SBT in serum reached 75.7 +/- 8.3 micrograms/ml at 0.25 hour after injection, and decreased to 2.3 +/- 0.7 micrograms/ml after 8 hours. The peak concentration of SBT in burn blister fluid was 13.5 +/- 1.8 micrograms/ml at 3 hours. The data obtained were analysed pharmacokinetically. Cmax of CPZ and SBT levels in burn blister fluid were calculated to be 30.4 micrograms/ml and 13.6 micrograms/ml, respectively. The AUC0-8 hrs. (area under the burn blister fluid concentration of drug-time curve between 0 and 8 hours after injection), absorption rate constant (ka) and therapeutic AUC (AUC where drug concentrations were above minimum effective concentration) of CPZ were calculated to be 194.0 micrograms.hr/ml, 1.52 hr-1 and 97.1 micrograms.hr/ml (0.3-11.1 hours), respectively. The AUC0-8 hrs. and ka of SBT were also calculated as 68.3 micrograms.hr/ml and 0.62 hr-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Blister↗
PubMed1987

PUVA-induced blisters, complement deposition, and damage to the dermoepidermal junction.

We followed the course of 56 patients receiving psoralen plus long-wave ultraviolet light (PUVA) therapy. Nonhemorrhagic blisters developed on clinically normal skin on the limbs of seven patients. Seeming to be related to friction and trauma, the blisters form as a result of damage to the basal and suprabasal layers. Perilesional skin specimens from all blistered patients contained granular deposits of C3 at the dermoepidermal junction, around the upper dermal blood vessels, or at both sites. The average time for initiation and complete formation of suction blisters was measured in 51 patients at different stages during the course of PUVA treatment. Blister separation was in the lamina lucida, with the pemphigoid antigen in the roof while the blister floor contained the lamina densa, laminin, and type IV collagen. This impaired dermoepidermal adhesion was a general phenomenon that occurred in all PUVA-treated patients. The mechanism remains to be determined.

Adult↗
PubMed1985

[Transfer of latamoxef into human burn blister fluid and its pharmacokinetic analysis].

Latamoxef (LMOX) (50 mg/kg) was administrated intravenously to burned patients over 1 hour period. Burn blister fluid and serum were taken during 8 hours after injection, and concentrations of LMOX in burn blister fluid and serum were determined by bioassay using E. coli as a test organism. The serum concentrations of LMOX were 170.8 +/- 30.6 micrograms/ml at 30 minutes, 227.0 +/- 19.8 micrograms/ml at 1 hour, 90.3 +/- 21.4 micrograms/ml at 2 hours, 52.9 +/- 14.6 micrograms/ml at 3 hours, 38.7 +/- 13.3 micrograms/ml at 4 hours, 25.1 +/- 8.1 micrograms/ml at 5 hours, 20.5 +/- 8.1 micrograms/ml at 6 hours, 13.0 +/- 5.5 micrograms/ml (mean +/- S.D., n = 5) at 8 hours after the injection. The LMOX concentrations in burn blister fluid were 36.9 +/- 32.8 micrograms/ml at 30 minutes, 77.5 +/- 42.2 micrograms/ml at 1 hour, 85.4 +/- 19.6 micrograms/ml at 2 hours, 76.4 +/- 18.5 micrograms/ml at 3 hours, 63.5 +/- 17.8 micrograms/ml at 4 hours, 54.9 +/- 17.1 micrograms/ml at 5 hours, 34.8 +/- 10.3 micrograms/ml at 6 hours, 25.2 +/- 4.8 micrograms/ml (mean +/- S.D., n = 7) at 8 hours after the injection. The data obtained were analysed pharmacokinetically. The serum levels were analysed by two-compartment model, and the LMOX levels in burn blister fluid were analysed by the model, in which blister was considered as a small part of the peripheral compartment. In results, Tmax and Cmax of LMOX levels in burn blister fluid were calculated as 1.81 hours and 90.6 micrograms/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1975

[Chemotactic activity in the fluid of bullous pemphigoid blisters].

By a modified Boyden technique, chemotactic activity was present in bullous pemphigoid blister fluids but was also present in the corresponding sera. Heat inactivation (56 degrees C for 30 minutes) only partially reduced the blister fluid chemotactic activity, but almost completely inhibited the activity present in pemphigoid sera. Control blister fluids exhibited some chemotactic activity, but in contrast to pemphigoid blister fluids, this activity was almost entirely abolished by heat inactivation. The chemotactic activity remaining in heat inactivated pemphigoid blister fluid was inhibited by N-CBZ-alpha-glutamyl-L-tyrosine and by antiserum to C5 but not with antiserum to C3. Our studies suggest that complement-dependent chemotactic activity is present in bullous pemphigoid blister fluids, findings which further implicate complement activation in the pathogenesis of this disease.

Blister↗
PubMedDate not supplied

Relationship between theoretical molecular weight and blister fluid/serum ratio of cytokines and five other molecules evaluated in patients with bullous pemphigoid.

Bullous pemphigoid (BP) blisters contain several molecules, some of which spread into the blisters from the interstitial fluid, while others are produced locally and migrate into the circulation. The calculation of the ratios between blister/serum concentrations may help to distinguish between these two types of molecules. The rules regulating the diffusion of the molecules have been described only in suction blisters, where the theoretical molecular weight (MW) represents one of the principal influencing factors. The aim of the present study was to analyse the relationship between theoretical MWs and the ratios of concentrations of several molecules evaluated both in sera and in blister fluids. Eight cytokines (interleukin-2, interleukin-3, interleukin-4, interleukin-5, interleukin-10, tumor necrosis factor-alpha, oncostatin-M and vascular endothelial growth factor), two acute phase reactants (alpha-1 acid glycoprotein, haptoglobin), albumin, one soluble membrane molecule with adhesion functions (sICAM-1) and the eosinophil cathionic protein (ECP) were measured in samples from 15 patients affected with BP by means of commercially available tests. The data suggest that the MW may influence the rate of diffusion throughout the blister, both in input and output directions, despite the discontinuity observed at the basement membrane level on the BP blister floor.

Acute-Phase Proteins↗
PubMedDate not supplied

Putative role of proteolysis and inflammatory response in the toxicity of nerve and blister chemical warfare agents: implications for multi-threat medical countermeasures.

Despite the contrasts in chemistry and toxicity, for blister and nerve chemical warfare agents there may be some analogous proteolytic and inflammatory mediators and pathological pathways that can be pharmacological targets for a single-drug multi-threat medical countermeasure. The dermal-epidermal separation caused by proteases and bullous diseases compared with that observed following exposure to the blister agent sulfur mustard (2,2'-dichlorodiethyl sulfide) has fostered the hypothesis that sulfur mustard vesication involves proteolysis and inflammation. In conjunction with the paramount toxicological event of cholinergic crisis that causes acute toxicity and precipitates neuronal degeneration, both anaphylactoid reactions and pathological proteolytic activity have been reported in nerve-agent-intoxicated animals. Two classes of drugs already have demonstrated multi-threat activity for both nerve and blister agents. Serine protease inhibitors can prolong the survival of animals intoxicated with the nerve agent soman and can also protect against vesication caused by the blister agent sulfur mustard. Poly (ADP-ribose) polymerase (PARP) inhibitors can reduce both soman-induced neuronal degeneration and sulfur-mustard-induced epidermal necrosis. Protease and PARP inhibitors, like many of the other countermeasures for blister and nerve agents, have potent primary or secondary anti-inflammatory pharmacology. Accordingly, we hypothesize that drugs with anti-inflammatory actions against either nerve or blister agent might also display multi-threat efficacy for the inflammatory pathogenesis of both classes of chemical warfare agent.

Animals↗