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At least 343 records · Page 19Linked to original sources

Studies of human leprosy lesions in situ using suction-induced blisters. 1. Cellular components of new, uncomplicated lesions.

The cellular contents of blisters induced by suction over new, uncomplicated leprosy lesions, and in the skin of cured, control patients, have been examined with enzyme- and immuno-histochemical staining over a period of 4 days. The total cellularity of the blisters varied over a wide range, not correlated with the type of leprosy. Mononuclear cells predominated at all times studied, with nearly equal percentages of monocytes and T lymphocytes. The T-helper: suppressor ratio was significantly greater in BT than in BL and LL lesions at 48 hr. Suction blisters offer a painless, quantitative, reproducible, multiple-sampling method for obtaining cells from the cutaneous infiltrates of leprosy for phenotyping or functional analysis.

Blister↗

Epidermal grafting using the tops of suction blisters in the treatment of vitiligo.

Fourteen patients with nondermatomal and 31 patients with segmental vitiligo were treated by epidermal grafting using the tops of suction blisters. Epidermis of the vitiliginous area was removed by a blister induced by methoxsalen plus ultraviolet A, and the tops of suction blisters were placed next to one another, resembling paving stones. Reepithelialization was completed in about two weeks, and skin color normalized in most cases about half a year later. Repigmentation persisted in most cases of segmental vitiligo, whereas loss of pigmentation occurred again in nonsegmental vitiligo. Scars were not observed on either the graft site or the donor site.

Blister↗

Comparison of topical antibiotic ointments, a wound protectant, and antiseptics for the treatment of human blister wounds contaminated with Staphylococcus aureus.

An open, randomized, human-model study was conducted to compare the effects of topical antibiotics, a wound protectant, and antiseptics on the rate of wound healing and bacterial growth using a modification of a method employing ammonium hydroxide-induced intradermal blisters inoculated with Staphylococcus aureus. Each volunteer in the study had six blister wounds (three per forearm) to which a triple antibiotic (neomycin, polymyxin B, bacitracin) ointment or one of four other test agents was applied twice a day. A control wound remained untreated. All wounds were covered with an occlusive dressing after treatment. The time to healing (100 percent epithelialization) was evaluated for each wound. Wounds were cultured for bacterial growth after two treatments. Contaminated blister wounds treated with the triple antibiotic ointment healed significantly faster (mean nine days) than wounds treated with any antiseptic and those receiving no treatment. Only the neomycin-polymyxin B-bacitracin combination effectively eliminated bacterial contamination of the wounds after two applications (within 16 to 24 hours after contamination with Staphylococcus aureus). The overall clinical appearance and healing rates of wounds treated with the triple antibiotic were ranked superior to all treatments (and no treatment) except the other antibiotic ointment in the study.

Administration, Cutaneous↗

Suction blister transplantation for leg ulcers.

Application of suction blister transplants to leg ulcers is an alternative symptomatic treatment to split-skin grafting, i.e. "pinch-grafting". Blisters are produced by the suction device Dermovac at a suction pressure of 250-300 mmHg for 1-2 hours. The blister-roofs are cut off at the periphery and placed on the granulation tissue of the ulcer. The healing time for leg ulcers was 10-14 days. Excellent epithelialization was seen in 10 out of 12 ulcers. The advantages of the method are, that it is easy to perform, no scarring is produced, and the procedure is painless.

Blister↗

IL-10 levels are decreased in psoriatic lesional skin as compared to the psoriatic lesion-free and normal skin suction blister fluids.

IL-10 is a cytokine produced by B and T-cells, monocytes and keratinocytes with pleiotropic effects, some of which are directed towards suppressing monocyte activities (anti-inflammatory cytokine). No information at the protein level is available concerning IL-10 in suction blister fluids from psoriatic skin, even if contrasting data have been reported on IL-10 mRNA of psoriatic biopsies and on the cytokine patterns of the T-cell clones, isolated from psoriatic skin. The IL-10 blister fluid concentrations in psoriatic lesions were compared to those found in the non-lesional skin of 14 patients effected with plaque-type psoriasis, and to those found in the skin of healthy controls (9 subjects sharing sex ratio and age with psoriatic patients). No difference in the IL-10 levels was found between non-lesional and control skin. In contrast, lower IL-10 levels were observed in blister fluids obtained from lesional psoriatic skin (p < 0.0005). The possible meanings of these results have been evaluated in the context of the mechanisms activating or maintaining the chronic inflammatory components of psoriasis.

Adult↗

Blistering on a squamous cell carcinoma graft site in a patient with bullous pemphigoid.

Bullous pemphigoid is a blistering disorder with blisters arising from normal, otherwise uninvolved tissue or from urticarial or erythematous plaques localized mainly on the trunk or upper extremities. Neoplasms, such as squamous cell carcinomas, have also been reported in patients with bullous pemphigoid. Large squamous cell carcinomas (greater than 8 cm in diameter) are best treated by surgical excision. We report a patient with bullous pemphigoid and squamous cell carcinoma who showed blisters on his graft site.

Blister↗

Blistering distal dactylitis caused by Staphylococcus aureus.

Blistering distal dactylitis is a superficial infection of the anterior fat pad on the volar surface of the distal portion of ordinarily a single finger. Although most commonly caused by group A beta-hemolytic streptococci, we report a case of blistering distal dactylitis caused by Staphylococcus aureus involving all the fingers and thumbs of a child. After results of a Gram's stain and culture established the diagnosis, the child responded rapidly to oral amoxicillin trihydrate/clavulanate potassium (Augmentin). Multiple fingers affected in blistering distal dactylitis may be a predictor of S. aureus as the causative agent.

Blister↗

Fracture blisters: a review of the literature.

Following orthopaedic trauma, fracture blister formation creates a disruption in skin integrity for the injured patient and unique care challenges for the nurse and physician. These blisters may delay surgery, alter the optimum treatment plan, promote wound infection, delay wound healing, and ultimately prolong recovery. This article presents a review of the current literature and includes a discussion of the anatomy of the skin, pathophysiology of fracture blisters, and a review of current research. The complications, prevention, treatment, and implications for nursing care are also examined.

Blister↗

Blister formation and skin damage induced by BaP1, a haemorrhagic metalloproteinase from the venom of the snake Bothrops asper.

Blister formation and skin damage can be induced by BaP1, a haemorrhagic metalloproteinase from the venom of the snake Bothrops asper. Pathological changes in the skin were investigated after intramuscular injections of Bothrops asper haemorrhagic metalloproteinase BaP1. Blisters developed within the first hour, with separation of epidermis from the dermal-epidermal junction, whereas acantholysis of epithelial cells was not observed. After the third hour there was ulceration with formation of a proteinaceous scab and inflammatory infiltrate. By 7 to 14 days there was evidence of a regenerative process in dermis and epidermis. Haemorrhage occurred in both dermis and hypodermis as a consequence of BaP1 injection, together with damage of sebaceous glands and an inflammatory reaction in which enlarged macrophages were the predominant cell type. Zymography assays showed the presence of several endogenous metalloproteinases in the exudate, skin homogenates and plasma. In addition, BaP1 was detected in exudates and plasma by immunoblotting. This technique also demonstrated the presence of components immunologically related to laminin and collagen type IV in exudates. It is suggested that BaP1, and probably endogenous matrix metalloproteinases, degrade some protein components at the dermal-epidermal junction, inducing the formation of blisters.

Animals↗

Antibodies to desmogleins 1 and 3, but not to BP180, induce blisters in human skin grafted onto SCID mice.

Pemphigus and bullous pemphigoid (BP) are blistering skin diseases associated with IgG autoantibodies to desmosomal and hemidesmosomal components. When autoantibodies to desmogleins 1 and 3 from patients with pemphigus foliaceus (PF) and pemphigus vulgaris (PV) or rabbit antibodies against the murine hemidesmosomal component BP180 are passively transferred into neonatal mice, they induce blisters in the skin of the mice. To develop an animal model that would duplicate the findings in the skin of the patients more closely, full-thickness human skin from healthy volunteers was grafted onto SCID mice. Injection of the purified IgG fraction from the serum of PF and PV patients led to subcorneal and suprabasal splits in the human grafts and human IgG was deposited intercellularly in the upper and lower layers of the epidermis, respectively. Interestingly, anti-BP180 autoantibodies purified from the serum of BP patients and from a rabbit immunized with recombinant human BP180 strongly bound to the basement membrane zone of the grafts (n=32), fixed murine complement, led to the recruitment of neutrophils to the upper dermis of the graft, but did not induce subepidermal blisters. We report a novel experimental model for PF and PV which should greatly facilitate further studies to dissect the immunopathological mechanisms in these diseases. Specifically, this model can be used to identify pathogenically relevant epitopes on human desmogleins 1 and 3 and to develop novel strategies for the treatment of pemphigus.

Animals↗

Fab fragments directed against laminin 5 induce subepidermal blisters in neonatal mice.

Patients with one form of cicatricial pemphigoid have IgG autoantibodies directed against laminin 5 (alpha3beta3gamma2), an adhesion protein in epidermal basement membrane. Anti-laminin 5 autoantibodies are not found in patients with other skin or mucosal diseases and hence serve as a specific marker for this autoimmune blistering disorder. The demonstration that experimental and patient anti-laminin 5 IgG are pathogenic in animal models indicated that such autoantibodies are central to disease pathophysiology. To investigate further the role of antibody valence and complement in triggering lesion formation in vivo, rabbit anti-laminin 5 (or normal, control) Fab fragments were passively transferred to neonatal BALB/c mice. Mice receiving anti-laminin 5 Fab fragments developed, in a dose-related fashion, circulating anti-basement membrane antibodies, deposits of immunoreactive rabbit IgG (but not murine C3) in epidermal basement membranes, and subepithelial blisters of skin and mucous membranes. Such alterations were not observed in mice treated with equivalent concentrations of normal rabbit Fab fragments. These studies demonstrated that neither complement activation nor cross-linking of laminin 5 in epidermal basement membranes was required for induction of subepidermal blister formation in this animal model of a human autoimmune bullous disease.

Animals↗

Ultrastructural studies in epidermolysis bullosa hereditaria. III. Recessive dystrophic types with dermolytic blistering (Hallopeau-Siemens types and inverse type).

Ultrastructural examination was performed in 42 biopsy specimens from 22 patients with the Hallopeau-Siemens types or with the inverse type of epidermolysis bullosa dystrophica recessiva. The patient group consists of 8 cases of the localized Hallopeua-Siemens type, 9 of the generalized Hallopeau-Siemens type and 5 of the inverse type. The origins of the biopsy specimens are involved, intact and experimentally frictioned skin from blister-predilected sites, as well as clinically normal skin from nonpredilection sites. It is confirmed that all the blisters initiate below the basal lamina. Anchoring fibrils are moderately to markedly decreased in most cases, while they are normal in 3 other cases. It is thought that secondary degradation of anchoring fibrils and/or collagen fibrils plays an important role in blistering mechanism in the Hallopeau-Siemens and inverse types of recessive dystrophic epidermolysis bullosa, whereas a primary aplasia of anchoring fibrils as causative defect has been out ruled.

Collagen↗

[Blistering autoimmune diseases of childhood].

Autoimmune blistering skin diseases are exceedingly rare in children. In most cases, they are characterized by circulating autoantibodies directed against adhesion structures of the skin which subsequently induce blistering at the dermoepidermal junction or intraepidermally. The most frequent paediatric immunobullous disease is linear IgA dermatosis; all others such as pemphigoid, epidermolysis bullosa acquisita, dermatitis herpetiformis and pemphigus are less common than in adults. In children, mucous membranes are involved more frequently. Recent advances in the identification of the autoantigens have improved diagnostic approach and therapeutic management of blistering diseases. In most cases, treatment requires systemic immunosuppression. With respect to the chronic course of the diseases and potential complications of treatment, cooperation between dermatologists and paediatricians seems advisable.

Autoimmune Diseases↗

Turning intermittent regimens into daily regimens using blister-packs. An exploration in murine tuberculosis.

SETTING: Blisterpacks might be used to present low cost intermittent regimens while maintaining an easily remembered daily frequency of opening blisters, by alternating blisters containing 2 of the drugs of a 4-drug regimen with blisters containing the remaining 2 drugs. OBJECTIVE: The efficacy of the alternating regimens was examined in murine tuberculosis. DESIGN: 2 weeks after infection with Mycobacterium tuberculosis H37Rv, groups of mice were treated with rifampicin (R) 15 mg/kg, isoniazid (H) 25 mg/kg, pyrazinamide (Z) 300 mg/kg, ethambutol (E) 100 mg/kg three times weekly (RHZE3); RH/ZE, an alternating regimen of RH on days 1, 3 and 5 of the week and ZE on days 2, 4 and 6, RZ/HE or RE/HZ. RESULTS: Spleen and lung bacillary counts at 7 and 12 weeks indicated large differences in the efficacy of the regimens: RZ/HE > RE/HZ > RHZE3 > RH/ZE. Serum assays showed that Rifampicin (RMP) levels were much lower after HRZE and slightly lower after RZ, RE and RH than after R alone, whereas levels were similar when R was given before the remaining drugs; also, the absorption of Z was slightly increased by R. A second experiment used the same 4 regimens but gave R before other drugs. The organ colony forming units counts at 6 and 12 weeks were then similar. A third experiment examined continuation phase regimens of R3, R2, R2H2 and R2H6 given after daily RHZ treatment for 4 weeks. It found R2H2 only slightly superior to R2H6 and R3 much better than R2. CONCLUSION: 1. Alternating initial phase regimens were as effective as conventional intermittent regimens. 2. R3H6 might be an optimal continuation phase regimen for blisterpacks.

Animals↗

The blistering diseases.

The intent and purpose of the authors is to familiarize the reader with the principles that govern the diagnosis and management of autoimmune mucocutaneous blistering diseases. The purpose was not to be all-inclusive but illustrative. There are several other blistering diseases that have not been discussed because of the limited scope of this article. Of these, toxic epidermal necrolysis, erythema multiforme, and the like warrant the same attention and early recognition. These are covered in different articles. For the same reasons, certain genetically linked blistering diseases have not been discussed.

Autoimmune Diseases↗

Mycophenolate mofetil: a new therapeutic option in the treatment of blistering autoimmune diseases.

BACKGROUND: Mycophenolate mofetil (MMF), an ester of mycophenolic acid (MPA), was approved by the Food and Drug Administration in 1995 and is currently primarily indicated for the prophylaxis of rejection in renal transplant patients. The drug seems also to be of value in the treatment of psoriasis and rheumatic arthritis. Recently there have been 6 reported cases of successful treatment of blistering autoimmune diseases with MMF in combination with high dose prednisone therapy. OBJECTIVE: On the basis of these reports we administered this new treatment regimen to several patients with blistering autoimmune diseases. Besides using a combination of MMF and high-dose prednisone we wanted to evaluate whether MMF monotherapy is also effective in the treatment of blistering autoimmune diseases. METHODS: We administered MMF to 5 patients who had severe pemphigus vulgaris or bullous pemphigoid. Two patients received MMF in combination with high-dose prednisone therapy and 3 patients received MMF monotherapy. To our knowledge, this is the first report of successful treatment of pemphigus vulgaris and bullous pemphigoid with MMF monotherapy. RESULTS: All patients were completely free of symptoms within 8 to 11 weeks of therapy. Patients who had received MMF monotherapy responded as well to treatment as those who received a combination of MMF and high-dose prednisone. CONCLUSION: Our experiences strongly suggest that MMF monotherapy may be effective for patients even with severe pemphigus vulgaris and bullous pemphigoid. In addition, MMF monotherapy, at least over the short term, offers the advantage of fewer side effects in comparison to immunosuppressive combination therapy and was well tolerated by our patients.

Aged↗

New and emerging therapies in the treatment of blistering diseases.

The autoimmune vesiculobullous diseases of the skin and mucous membranes are a fascinating group of diseases characterized by blisters of the skin and mucous membranes. These diseases are among the most intriguing, well-characterized, and potentially serious skin diseases known. In recent years, there has been major progress made in the understanding of their pathophysiology, in the development of new diagnostic techniques and of new therapeutic approaches. These advances have placed the autoimmune blistering diseases of the skin and mucous membranes at the forefront of dermatologic advances in the late twentieth century. This article discusses several of the most important autoimmune blistering disease, including bullous pemphigoid, mucous membrane pemphigoid (formerly known as cicatricial pemphigoid), epidermolysis bullosa acquisita, linear IgA bullous dermatosis, pemphigus and paraneoplastic pemphigus, with particular emphasis on the use of new and emerging therapeutic approaches.

Epidermolysis Bullosa↗

New immunomodulating drugs in autoimmune blistering diseases.

The autoimmune blistering diseases are a fascinating group of diseases characterized by the presence of blisters involving the skin and mucous membranes. Understanding of the diagnosis, pathophysiology, and advances in treatment of these diseases has grown enormously in recent years. In this article, the author discusses the major clinical and immunopathologic findings in bullous pemphigoid, mucous membrane pemphigoid, epidermolysis bullosa acquisita, linea IgA bullous disease, and pemphigus. The article focuses on the therapeutic management of patients with autoimmune blistering diseases, including the appropriate treatment of patients, with particular emphasis on the use of immunomodulating and immunosuppresive agents.

Adjuvants, Immunologic↗