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At least 181 records · Page 10Linked to original sources
PubMed2000

Blisters on psoriatic lesions treated with TL-01 lamps.

BACKGROUND: Asymptomatic blisters on psoriatic plaques are an uncommon adverse effect of TL-01 (UVB narrow-band 312 nm) phototherapy. OBJECTIVE: We report 7 new cases aiming to clarify the pathogenesis. METHODS: Blisters were biopsied at different times after onset. Blood porphyrins and antibodies to nuclear antigens and the cell surface of keratinocytes were investigated. RESULTS: We observed 7 asymptomatic blistering eruptions strictly limited to recovering psoriatic plaques. Biopsies taken within 24 h showed junctional detachment and apoptotic necrosis of basal keratinocytes. After 48 and 72 h, the blisters were intraepithelial, due to basal cell regeneration, and were no longer evident at 96 and 120 h. Dermal inflammation was always mild. Direct immunofluorescence tests as well as stainings for p53 protein did not show substantial changes. Blood investigations were negative. CONCLUSIONS: TL-01 blisters are caused by the quick reduction of acanthosis and desquamation before defensive mechanisms, i.e. the increase in the thickness of the stratum corneum and pigmentation, develop. However, the pathogenetic mechanisms of apoptosis of keratinocytes remain unknown.

Adolescent↗
PubMed1984

Plasma and skin blister fluid levels of cefotiam and cefmenoxime after single intramuscular application of 1 g in gonorrhea.

To predict the clinical efficacy of a new antibiotic in uncomplicated gonorrhea, data pertinent to its pharmacokinetics in man are needed. Before starting clinical trials on cefotiam and cefmenoxime, 1 g of each antibiotic was administered intramuscularly as a single dose to 5 healthy volunteers. Both blood and skin blister fluid samples (obtained by suction and cantharides blistering) were repeatedly taken. Peak plasma levels amounted on average to 24.8 and 48.2 micrograms/ml, respectively. 6 h after dose still average plasma concentrations of 3.4 and 6.52 micrograms/ml were found. Suction blister fluid levels essentially paralleled plasma levels, whereas cantharides blister fluid levels increased and decreased more slowly than plasma levels. Cefotiam penetrated more readily into suction blister fluid than cefmenoxime as obtained from area ratios. Thus, the chosen dosage regimens considered apt for gonorrhea led to high initial as well as long-standing drug levels. And this does not only hold true for the plasma. Facing their good in vitro activity on Neisseria gonorrhoeae, cefotiam and cefmenoxime well deserve further studies in this field including clinical trials.

Adult↗
PubMed2002

Managing blisters in competitive athletes.

Friction blisters can have a negative effect on an individual's ability to perform his or her sport or duties. In a recent study, 69% of soldiers participating in a 20-km road march were found to have blisters, 10% of whom required medical intervention. Blistering of the feet is one of the most common injuries sustained by runners while training and racing. Although most blisters are minor and can be treated conservatively, others can lead to intense pain, cellulitis, and even sepsis. The best way to treat friction blisters is to prevent them; however, if they do occur, timely and effective treatment will help prevent the complications that can impede athletic performance.

Blister↗
PubMed2005

Pemphigoid nodularis: two case studies and analysis of autoantibodies before and after the development of generalized blistering.

We report 45- and 61-year-old women with generalized prurigo nodularis-like eruption whose clinical, histologic and immunopathologic features were consistent with the diagnosis of pemphigoid nodularis. In one case, nodular lesions preceded the onset of generalized blistering by two years and in the other, no definite blister nor erosion was seen except for some appearing on the soles during the course of the disease. Western immunoblotting of EDTA-separated epidermal extracts revealed that the 230-kD bullous pemphigoid (BP) antigen was recognized by circulating autoantibodies in the patient sera, but the 180-kD BP antigen was not. The 180-kD BP antigen was recognized weakly by immunoblotting of the 180-kD BP antigen NC16a domain fusion protein, which shows high detection sensitivity. These findings suggested that weak reactivity of autoantibodies with either whole or a part of the 180-kD BP antigen molecule in some way accounts for negligible or localized blister-formation in this disorder. However, no particular change was noted in the reactivity with 180-kD BP antigen between the patient serum obtained before and after the development of generalized blistering. It is possible that different factors from the changes in serum reactivity with BP antigens may be involved in initiating generalized blistering.

Autoantibodies↗
PubMed1992

Suction blister fluid histamine in fixed drug eruption.

The histamine concentration was measured from suction blister fluid obtained from normal and lesional skin of 8 patients with fixed drug eruption (FDE) caused by phenazone salicylate and from that of 2 healthy control subjects. In blister fluid samples obtained before peroral challenge with phenazone salicylate, the histamine concentrations were below 5 nmol/l both in uninvolved skin and in sites of previous FDE lesion (sample 0). After challenge, samples were taken from the incipient reaction that was visible after an average of 155 min. Histamine levels were significantly elevated in the blister fluid of 2 out of 8 FDE lesions (200 and 640 nmol/l) but in none of the uninvolved skin (sample 1). Two hours later (sample 2) the histamine levels were elevated in both uninvolved (mean 51.4 nmol/l) and lesional skin (mean 168 nmol/l). After 24 h (sample 3) the corresponding mean value was 25.4 nmol/l for uninvolved skin and 108 nmol/l for lesional skin. The histamine values in the blister fluid from FDE lesions in samples 2 and 3 were significantly higher (p less than 0.05) than those in the control blisters of uninvolved skin. An elevation of histamine levels comparable to that in the uninvolved skin of FDE patients was seen in the 2 healthy control subjects studied. The present study provides direct evidence of early release of histamine from mast cells or basophils in FDE and suggests that histamine is one of the mediators of clinical symptoms of FDE.

Adolescent↗
PubMed1992

Comparison of plasma prekallikrein levels in human skin blister and chamber fluids from volunteer subjects and psoriatic patients.

Suction blisters were successfully raised on lesional, perilesional and non-lesional skin of psoriatic patients. Similar blisters were created on the skin of volunteer subjects. A specific method has been established for the measurement of plasma prekallikrein, and validated for blister fluid, skin chamber fluid, plasma and synovial fluid. Combined levels of plasma prekallikrein and its active form were compared in blister fluids obtained from psoriatic patients and the volunteers. Significantly higher values for plasma prekallikrein were found in the non-lesional blister fluids of psoriatic patients when compared to the volunteer subjects.

Blister↗
PubMed1992

Basement membrane and fibroblast aberration in blisters at the donor, graft, and spontaneously healed sites in patients with burns.

BACKGROUND AND DESIGN: Blisters that developed on spontaneously healed wounds and grafts in 13 patients with burns were analyzed by light, fluorescence, and electron microscopy. RESULTS: Blisters developed on the dermal side of the dermoepidermal junction and occurred more frequently in donor site and healed mesh graft than in split-thickness sheet graft. The four major components of the basement membrane zone (bullous pemphigoid antigen, laminin, type IV collagen, and epidermolysis bullosa acquisita antigen) were reduced in quantity and irregularly deposited at blister sites. Immediately adjacent to the blisters, epidermolysis bullosa acquisita antigen appeared normal in quantity, while laminin, type IV collagen, and bullous pemphigoid antigen levels appeared slightly reduced. Mononuclear infiltrates and autoantibodies were not detected by light microscopy or direct-indirect immunofluorescence, respectively. Ultrastructurally, adjacent dermal fibroblasts demonstrated swollen rough endoplasmic reticulum and vacuolization. CONCLUSIONS: We speculate that blister development in patients with burns is related to defective reorganization of the basement membrane zone in association with dermal fibroblast aberration during wound healing.

Adolescent↗
PubMed1986

Hyaluronate in suction blisters from patients with scleroderma and various skin disorders.

With a specific radioassay hyaluronic acid (hyaluronate) concentrations have been determined in suction blister fluid from abdominal skin and serum. Healthy subjects, patients with acrosclerosis, CRST, mucinosis and urticaria had 0.8-5.6 micrograms/ml of hyaluronate in their suction blisters, which is about 100 times more than the serum level. Increased concentrations were noted in blister fluid from patients with active lesions of systemic and localized scleroderma as well as lichen sclerosus. Here the increase could be due to an increased production of hyaluronate in the dermis. High levels of hyaluronate were, however, also found in blister fluid from patients with other types of inflamed skin. An increased leakage into the blister of hyaluronate from the dermis, probably through the lymph vessels, therefore seems best to explain the high concentrations of hyaluronate.

Blister↗
PubMed1986

Study of elastase-type activity in blister fluids of recessive dystrophic epidermolysis bullosa.

Recessive dystrophic epidermolysis bullosa (RDEB) is characterized clinically by blister formation due to minor trauma and ultrastructurally by a progressive disappearance of anchoring fibrils at the dermoepidermal junction and of the oxytalan-type fibers which belong to the elastic fiber system. In this study, we determined the elastase-type activity in blister fluid obtained from 8 patients suffering from RDEB as compared to the suction fluid of experimental blisters in a healthy person and to the blister fluid of a patient suffering from epidermolysis bullosa simplex. One patient with dominant dystrophic epidermolysis of the albopapuloid type was also studied. Seven of the eight children with RDEB showed highly elevated values. The eighth child, treated with etretinate, as well as the patient suffering from dominant epidermolysis bullosa had moderately increased values. The determination of elastase-type activity in the blister fluid could therefore be useful to establish the differential diagnosis of recessive dystrophic epidermolysis bullosa.

Blister↗
PubMed1987

Histogenesis of UV light-induced blister formation.

Histological examination of ultraviolet light (UVL)-induced blister formation in guinea pig skin is reported. Light and electron-microscopic examination was performed on skin exposed to single and multiple exposures of a large dose of UVB. In light microscopy, intracellular edema was prominent, especially in the lower part of the epidermis, where it developed into a blister. It seemed to be a subepidermal bulla. The PAS-positive basement membrane was observed at the floor of the blister. The positive Nikolsky's sign seemed to be due to a separation between the degenerated and regenerated epidermis. Electron microscopy revealed a marked intercellular as well as intracellular edema and well-preserved desmosomes. The basal lamina was always located at the floor of the blister. The difference in UVL-induced blister formation between normal and pathological conditions is discussed.

Animals↗
PubMed1979

[Ultrastructure of epidermolyses with junctional blister formation (author's transl)].

Junctional blister formation is the common feature of four clinically different types of inherited epidermolyses with atrophies but lack of scarring which, as a group, have been termed epidermolysis bullosa atrophicans. The Herlitz type is the most common one among them. Based on a material of 24 cases aged 2 days to 42 years at the time of biopsy, ultrastructural data on the pathomorphogenesis are reported. Blisters form in the dermo-epidermal junction area between the basal lamina and the basal cell plasma membrane. A well-developed basal lamina-anchoring fibrils complex covers the blister floor. Hypoplasia of hemidesmosomes precedes blister formation and is a constant finding in intact junction area without any other signs of disturbances. It is, therefore, regarded as a causal factor in the pathogenesis. Nail loss as a result of junctional separation within the nail bed, secondary changes in older blisters and formation of slowly healing granulation tissues are also reported.--Early diagnosis is made available by electron microscopy as shown in out early childhood cases. Genes coding for junctional epidermolyses seem to be far more frequent than those coding for the scarring or dystrophic types.

Adolescent↗
PubMed1984

[Evaluation of the extravascular distribution of cefotiam (SCE 963) by the skin blister technic].

Extravascular diffusion of cefotiam was studied by a suction blister technique. Maximal cefotiam concentration in blister fluid (18.4 +/- 6.4 micrograms X ml-1) was found one hour after intravenous injection of a 1 g bolus. The area under the curve (AUC) of blister fluid concentrations was 35.4 micrograms X ml-1. Apparent elimination half-life from blister fluid was 0.72 hour. The AUC plasma/AUC blister fluid ratio approximated 1.

Adult↗
PubMed1984

[Transfer of cefmenoxime to burn blister fluids].

Transfer of cefmenoxime (CMX) into the burn blister fluids was studied in 10 burned patients with 2 administrated doses (25, 50 mg/kg). CMX concentrations in serum and burn blister fluid after 1 hour intravenous drip infusion were measured using Proteus mirabilis ATCC 21100 as the test organism grown in the DST agar medium. In the case of CMX 25 mg/kg dose, the peak serum concentration was observed 61.5 micrograms/ml at 1 hour, while the peak burn blister fluid concentration was observed 15.2 micrograms/ml at 2 hours. Pharmacokinetic parameters of serum concentration calculated were 1.02 hours as half-life (beta) and 0.42 L/kg as distribution volume, respectively. In the case of CMX 50 mg/kg dose, the peak serum concentration was observed 122.0 micrograms/ml at 1 hour and the peak burn blister fluid concentration was observed 40.8 micrograms/ml at 2 hours. Pharmacokinetic parameters of serum concentration calculated were 1.27 hours as half-life (beta) and 0.55 L/kg as distribution volume. From this study, the dose dependency between 25 mg/kg dose and 50 mg/kg dose in serum and in burn blister fluid is recognized.

Adolescent↗
PubMedDate not supplied

Using the nursing process to solve a problem: post-op tape blisters.

ET nursing consultation was requested for the treatment of ten cases of tape blisters within six months, the majority of which were post-op following hip surgery. When the ET nursing staff was asked to develop a standard treatment protocol for these blisters, they used the nursing process. They identified the problem, assessed the situation, planned and implemented a response, and evaluated the results in an ongoing manner. It was then theorized that lack of "stretch" in the tape might be causing the tape blisters. After five stretch tapes were assessed for ease of removing the paper backing, handling, application, flexibility, and adhesion, one tape was preferred by the operating room and nursing unit staffs and was put into routine use in October 1992. No further blisters have been noted since this change was made. By using the nursing process, the authors ultimately eliminated post-op tape blisters in the facility.

Adhesives↗
PubMed1993

[Diffusion of lipid fractions through the barrier of cantharidin blisters in hyperlipidemias under conditions of clofibrate and rutinosid interaction].

Diffusion of lipid fractions from blood to fluid in blister induced by cantharidal ointment, applied on the forearm skin, was studied in 54 patients, thereof 18 with normlipidemia, 13 having type II hyperlipidemia, 23 with type IV hyperlipidemia. Concentrations of triglycerides, phospholipids, free fatty acids, total cholesterol, HDL-cholesterol and LDL--cholesterol were studied in blood and fluid before treatment, 10 days after applying clofibrate, 20 days after clofibrate application, and 10 days following the application of rutinosid, i.e. upon completion of therapy. After the treatment it was observed that in all the patients the concentration of lipid fractions in blood was lowered, except for HDL-cholesterol, the level of which was elevated, as was the concentration of all the fractions in the blister fluid. Lipid concentration in serum, with the exception of free fatty acids, was invariably higher than in blister fluid. Free fatty acids, LDL-cholesterol and HDL-cholesterol diffused from blood to fluid in a greater percentage. Lipid fraction concentration in fluid depended mainly on the concentration of HDL-cholesterol and triglycerides in the blood. In normlipidemia, the highest percentage of lipid fractions was diffused to blister fluid; the percentage was lower in type IV hyperlipidemia, the lowest being in type II hyperlipidemia. Clofibrate hypolipemia action correlated best with with HDL-cholesterol and triglyceride activity. After the treatment, the elevated diffusion of all the fractions from blood to blister fluid was, in my opinion, consistent with lipid metabolism, venoruton, as vessel tightening drug, may play a protective role in relation to endothelia in hyperlipidemia.

Administration, Cutaneous↗
PubMed1994

Foot blister risk factors in an ROTC summer camp population.

Data that establish risk factors for foot blister morbidity among ROTC cadets at summer camp are presented. The subjective blister attack rate was 42.1 per 100 cadets. Women had a relative risk of 1.6 that of men (p < 0.001). Cadets with a history of blisters in the 2 years before camp had an increased relative risk of blister formation. Cadets who reported wearing their boots less than 20 hours per week during the 2 weeks immediately before camp had elevated risk. Other factors are examined. These data suggest that the foot must become conditioned to its footwear to prevent blister formation.

Adult↗
PubMed1996

Deposition of eosinophil granule proteins precedes blister formation in bullous pemphigoid. Comparison with neutrophil and mast cell granule proteins.

Eosinophils, neutrophils, and mast cells have all been implicated in the pathogenesis of bullous pemphigoid (BP). To comparatively characterize the involvement of these cells in BP, 10 lesional skin biopsy specimens were identified retrospectively and studied for tissue localization of eosinophil, neutrophil, and mast cell granule proteins. Subsequently, multiple skin biopsies of lesions in various developmental stages were obtained from 3 patients with untreated BP. Involved and uninvolved skin specimens were also obtained from 2 patients. Using indirect immunofluorescence, retrospectively identified lesions showed eosinophils and extracellular granule protein deposition prominently in areas of blistering. Evolving lesions showed eosinophil granule protein deposition in all stages but was most marked in early erythematous and prebullous (urticarial) lesions and was minimal in uninvolved skin. Vascular cell adhesion molecule-1, E-selectin, and P-selectin were detected on vessels and very late activation antigen-4 was detected on mononuclear cells and eosinophils by immunoperoxidase staining of lesions. Eosinophil granule proteins were increased in the peripheral blood, urine, and blister fluid. Blister fluids caused increased eosinophil survival that was inhibited by antibodies to interleukin-5 and interleukin-3. Although neutrophil and mast cell infiltration was observed, extracellular granule protein deposition from these cells was minimal except in two specimens. These results demonstrate that eosinophils infiltrate and deposit granule proteins early in the development of BP lesions, that eosinophil-activating cytokines are present in blister fluid, and that eosinophil-selective adhesion molecules are present. These studies strongly support a role for eosinophils in blister formation in BP.

Aged↗
PubMed1990

Oedemerid blister beetle dermatosis: a review.

Blister beetle dermatosis is a distinctive vesiculobullous eruption that occurs after contact with three major groups of beetles (Order: Coleoptera). It is caused by a vesicant chemical contained in the body fluids of the beetles. The smallest and least known family is the Oedemeridae. Although there are few references in the medical literature, blister beetle dermatosis caused by oedemerids may be more common and widespread than currently recognized. The best known family is the Meloidae with numerous species worldwide causing blistering. The vesicant chemical in both Oedemeridae and Meloidae is cantharidin. The third group of blister beetles includes species of the genus Paederus (Family: Staphylinidae). The clinicopathologic picture differs because this genus contains a different vesicant agent, pederin. The clinicopathologic features of oedemerid blister beetle dermatosis are described. The world medical and relevant entomologic literature is reviewed.

Animals↗